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PubMed2026

Quantification of appetite-regulating hormones in children with hypothalamic and common obesity.

CONTEXT: The pathophysiology of hypothalamic obesity (HyOb) remains incompletely understood with no effective treatments. OBJECTIVE: We examined differences in appetite-regulating hormone concentrations between patients with HyOb, common obesity, and lean controls. DESIGN: Multiway cross-sectional case-control study of patients aged 2 through 19 years. SETTING: Two tertiary pediatric endocrinology centers. PATIENTS: Cases were obese (body mass index [BMI] > +2 SD score [SDS], "HyOb") and lean ("HyLean") patients with congenital (septo-optic dysplasia) or acquired (suprasellar brain tumor) hypothalamic disorders. Controls had common obesity ("Ob") or nonhypothalamic disorders and normal BMI ("Lean"). MAIN OUTCOME MEASURES: Relationships between the Dykens' Hyperphagia Questionnaire Score (DHQS), plasma or serum concentrations of leptin, insulin, α-melanocyte stimulating hormone (αMSH), brain-derived neurotrophic factor, oxytocin, acylated ghrelin, agouti-related peptide and copeptin, and BMI SDS. RESULTS: Dykens' Hyperphagia Questionnaire Score did not differ between HyOb and Ob patients (24 [17-34] vs 24 [18-31]) but correlated with BMI SDS in patients with hypothalamic disorders (P = 0.02). HyOb and Ob patients exhibited similarly increased anorexigens (insulin, leptin) and decreased orexigens (ghrelin, agouti-related peptide) compared to HyLean and Lean patients. The rate of BMI increase was independently associated with lower αMSH (β = -0.23 [-0.36 to -0.11], P = .0007) and ghrelin (β=-0.004 [-0.01 to 0.00], P = .001) concentrations, suggesting that αMSH replacement may be a therapeutic target for HyOb. HyLean patients demonstrated intermediate insulin responses to glucose compared to other subcohorts. CONCLUSION: In our cohort, patients with HyOb appeared indistinguishable from Ob in terms of their appetite and appetite-regulating neuroendocrine circuitry. Higher αMSH concentrations are associated with reduced weight gain and may be a target for therapeutic intervention.

alpha-MSH↗

PubMed2026

Exogenous gibberellin promotes lateral branch development in stumping Pinus yunnanensis by regulating endogenous hormones and TCP genes.

While plant stumping can break apical dominance, promote lateral branching, and thereby increase yield, a significant technical challenge remains in further enhancing the coppicing regrowth capacity after stumping. This study used one-year-old Pinus yunnanensis Franch seedlings as subjects. Through exogenous application of gibberellin 3 (GA3) and Paclobutrazol (PAC), it investigated the regulatory role of gibberellin (GA) in sprouting and identified TCP genes related to branching within the GA pathway. Results indicate that exogenous hormone treatments altered endogenous hormone levels in P. yunnanensis seedlings. Exogenous GA3 treatment significantly increased endogenous IPA, ABA, GA3, GA1, SA, and SAG content. Correlation analysis with sprout number revealed a positive relationship between endogenous hormones and sprout number, indicating that exogenous GA3 significantly influenced sprout number. After hormone application, the cumulative number of sprouts increased with seedling age across all treatments. Therefore, to further investigate whether changes in sprout number were caused by gene alterations in the GA signaling pathway, this study analyzed the GA signaling pathway and its associated transcription factors. Fifteen TCP family members were screened from the P. yunnanensis transcriptome, phylogenetically classified into Class I and Class II subfamilies. Conserved motif sites within the Class II family co-occurred, exhibiting high conservation. Genes from the Class II subfamily were cloned, and their differential expression across various tissues was analyzed via real-time quantitative PCR. Expression patterns under different hormone treatments were also examined. Our results reveal that PyTCP4, PyTCP6, and PyTCP20 are significantly upregulated by PAC (a GA synthesis inhibitor) and show strong negative correlations with sprouts number, while GA3 treatment partially alleviates this effect. These findings provide direct evidence that TCP transcription factors act as repressors of shoot branching, linking their hormone-responsive expression to the regulation of sprouts formation in P. yunnanensis. These results indicate that TCP transcription factors play a crucial role in shoot and root emergence, with their expression influenced by exogenous hormones, thereby affecting the growth and development of emerging shoots and roots. This provides a reference and basis for analyzing the expression patterns and functions of TCP genes in P. yunnanensis, facilitating further research into their functions.

Gibberellins↗

PubMed2024

Mechanistic insights into steroid hormone-mediated regulation of the androgen receptor gene.

Expression of the androgen receptor is key to the response of cells and tissues to androgenic steroids, such as testosterone or dihydrotestosterone, as well as impacting the benefit of hormone-dependent therapies for endocrine diseases and hormone-dependent cancers. However, the mechanisms controlling androgen receptor expression are not fully understood, limiting our ability to effectively promote or inhibit androgenic signalling therapeutically. An autoregulatory loop has been described in which androgen receptor may repress its own expression in the presence of hormone, although the molecular mechanisms are not fully understood. In this work, we elucidate the mechanisms of autoregulation and demonstrate, for the first time, that a similar repression of the AR gene is facilitated by the progesterone receptor. We show that the progesterone receptor, like the androgen receptor binds to response elements within the AR gene to effect transcriptional repression in response to hormone treatment. Mechanistically, this repression involves hormone-dependent histone deacetylation within the AR 5'UTR region and looping between sequences in intron 2 and the transcription start site (TSS). This novel pathway controlling AR expression in response to hormone stimulation may have important implications for understanding cell or tissue selective receptor signalling.

Receptors, Androgen↗

PubMed2026

Aldosterone suppresses Na+/H+ exchanger-3 expression through miR-204-5P-mediated posttranscriptional regulation in distal colon.

Na+/H+ exchanger-3 (NHE3) is a major mediator of electroneutral NaCl absorption in the intestine and colon. In the distal colon, chronic aldosterone exposure suppresses NHE3 expression, but the molecular mechanism responsible for this regulation remains unclear. Here, we tested whether aldosterone represses NHE3 through microRNA-dependent posttranscriptional regulation. Transcriptomic analysis of distal colon from dietary Na+-depleted rats identified miR-204-5P (miR-204-5P) as markedly upregulated. Aldosterone increased miR-204-5P abundance and concomitantly reduced NHE3 mRNA, protein expression, and transport activity in rat and human distal colonic epithelium and in SK-CO15 cells. Bioinformatic and reporter analyses identified a conserved miR-204-5P binding site within the NHE3 3'-untranslated region, and miR-204-5P mimic transfection markedly suppressed NHE3 expression and transport activity without affecting other Na+/H+ exchanger isoforms. These findings identify a previously unrecognized aldosterone-microRNA signaling pathway that mediates chronic repression of NHE3 and provide new insight into hormonal regulation of colonic Na+ absorption.NEW & NOTEWORTHY This study identifies a previously unrecognized aldosterone-microRNA signaling mechanism regulating colonic Na+ absorption. We demonstrate that aldosterone induces miR-204-5P, which directly targets the NHE3 3'-untranslated region and suppresses NHE3 expression and transport activity in distal colonic epithelium. These findings reveal a microRNA-mediated pathway linking mineralocorticoid signaling to long-term inhibition of electroneutral NaCl absorption, providing new insight into hormonal regulation of intestinal electrolyte transport.

Animals↗

PubMed2026

Epigenome-wide placental methylation landscapes in relation to antenatal depressive symptoms.

Antenatal depressive symptoms (ADS) are common during pregnancy and are linked to adverse maternal and offspring neurodevelopmental outcomes. The placenta plays a central role in maternal-fetal communication and may function as an epigenetic sensor of maternal psychological stress. However, placental epigenetic signatures associated with ADS remain poorly understood. This study investigated epigenome-wide placental DNA methylation patterns associated with ADS in an Indian cohort. Placental samples were collected at delivery from women recruited in early pregnancy into the STRiDE cohort. Depressive symptoms were assessed at 24-28 weeks' gestation using the Patient Health Questionnaire-9 (PHQ-9). Participants were classified as controls (PHQ-9 ≤ 4; n = 53) or ADS (PHQ-9 > 4; n = 54). Genome-wide DNA methylation profiling was performed using the Illumina Infinium MethylationEPIC array. Epigenome-wide association analysis identified no CpG sites that remained statistically significant after Benjamini-Hochberg FDR correction. Top nominal CpGs showed medium-to-large effect sizes for ADS. Exploratory analyses of the top nominally associated CpGs annotated to genes including TAP2, LRCH1, SLITRK2, RASSF1 and IL3 implicated in immune regulation, cellular signalling and neurodevelopment. Gene enrichment analysis suggested the involvement of biological processes and pathways related to synaptic organization, ion transport, Hippo signalling, and thyroid hormone regulation. In conclusion, the study findings provide preliminary evidence of DNA methylation signatures linked to potential candidate genes and biological pathways that may be relevant to ADS, supporting the need for validation in larger independent cohorts and functional experimental studies.

Asian Indians↗

PubMed2026

Integrated phenotype, endogenous hormones and transcriptome analysis revealed the mechanism of response of Phoebe bournei seedlings to shade signals.

Understory tree seedlings are subjected to prolonged shading stress imposed by the canopy foliage, which significantly impedes their growth. A hallmark of shaded environments is a reduced red to far-red light ratio (R: FR). This study elucidates the physiological and molecular responses of the endangered tree species Phoebe bournei to shading signals. Seedlings were exposed to white light (control) and simulated shading environments with R: FR ratios of 1.5, 0.8, and 0.2. The findings reveal that an increase in the proportion of far-red light significantly enhances seedling height, root-collar diameter, internode length, petiole length, leaf surface area, and leaf biomass. Differentially expressed genes (DEGs) in each treatment group predominantly enrich pathways associated with hormone signaling, stress responses, and photosynthesis. Validation experiments demonstrate that shading promotes the activity of Rubisco and RCA enzymes, total chlorophyll (Chl) accumulation, and elevated levels of hormones including indole-3-acetic acid (IAA), gibberellic acid (GA3), salicylic acid (SA)/methyl salicylate (MeSA), cytokinins (CK), abscisic acid (ABA), and jasmonic acid (JA). Weighted Gene Co-expression Network Analysis (WGCNA) identifies seven hub genes linked to photosynthesis and plant hormone regulation: MYB, KSC, SUAR, CESA POD, CESA, and SAUR. Collectively, shading signals induce P. bournei seedlings to elongate their stems and petioles, enhance photosynthetic enzyme activity, and accumulate specific hormones, with pertinent genes actively participating in light signal transduction. This research sheds light on the shading response mechanism of P. bournei, providing a robust theoretical framework for the breeding of shade-tolerant trees and the conservation of endangered species.

Transcriptome↗

PubMed2026

Mechanistic analysis of rice caryopsis morphogenesis regulated by exogenous hormones and related precursor substances under blue light conditions.

Rice caryopsis morphogenesis is regulated by light signals and hormonal networks. However, the mechanism by which exogenous hormones and related precursor substances modulate rice caryopsis morphogenesis under blue light remains elusive. In the present study, we aimed to elucidate the molecular mechanisms underlying the regulatory effects of exogenous phytohormones and related precursor substances on caryopsis development at 10 days after pollination (10 DAP) in the japonica rice cultivar 'Chujing 27' under blue light conditions. Results showed that tryptamine treatment increased caryopsis cell volume, thereby significantly driving caryopsis expansion; meanwhile, it markedly enhanced the activities of TDC and TAA, the key rate-limiting enzymes mediating the conversion of tryptophan to auxin, leading to a significant elevation in endogenous auxin content (P < 0.05). In comparison, exogenous auxin treatment significantly boosted carbohydrate accumulation and the activities of associated metabolic enzymes (P < 0.05). Integrated transcriptomic and metabolomic analyses revealed that tryptamine treatment led to significant enrichment of the starch and sucrose metabolic pathway, and drove the coordinated enhancement of carbon metabolic flux and auxin biosynthesis by upregulating key auxin biosynthetic genes (e.g., TAA1) and repressing auxin oxidative degradation. Genes Os04g0531100, Os03g0266100 and Os11g0221200 identified by weighted gene co-expression network analysis (WGCNA) may serve as important candidate targets regulating rice caryopsis morphology and physiological traits under blue light conditions. This study first uncovers the critical function of the "tryptamine-auxin axis" in regulating rice caryopsis development under blue light, laying a theoretical foundation for regulating caryopsis morphogenesis via exogenous hormones and their precursors.

Oryza↗

PubMed2026

Genome-wide characterization of BraABCB transporters reveals their potential roles in hormone responses in Brassica rapa var. parachinensis.

Thirty-six BraABCB genes were identified in Brassica rapa var. parachinensis; expression and interaction analyses suggest BraABCB27 and BraABCB28 as hormone-responsive candidates associated with BRI1-related proteins. ABCB transporters are ATP-dependent membrane proteins that mediate the transport of diverse substrates, including phytohormones, and play important roles in plant development and environmental adaptation. Previous studies in Arabidopsis have shown that several ABCB proteins participate in phytohormone transport, including auxin and brassinosteroid transport, whereas the functions of their homologs in Brassica rapa var. parachinensis remain poorly understood. In this study, 36 BraABCB genes were identified and classified into four phylogenetic groups. Conserved domain analysis showed that BraABCB proteins contain typical nucleotide-binding domains and transmembrane domains. Chromosomal distribution, collinearity, and Ka/Ks analyses suggested that the BraABCB family is evolutionarily conserved and mainly subject to purifying constraints. Promoter analysis and RT-qPCR assays of selected Group IV BraABCB genes revealed diverse expression patterns and responses to drought, high temperature, brassinolide, and indole-3-acetic acid treatments. Subcellular localization assays showed that selected Group IV BraABCB proteins exhibited predominant plasma membrane localization. Notably, BraABCB27 and BraABCB28, two close AtABCB1/AtABCB19-related homologs, showed detectable physical associations with BRI1-related proteins in BiFC and split-ubiquitin yeast two-hybrid assays. Together, these results provide a genome-wide characterization of the BraABCB gene family and identify BraABCB27 and BraABCB28 as candidate genes for future studies of their possible associations with BR-related membrane processes and hormone-regulated growth responses in B. rapa var. parachinensis.

Plant Growth Regulators↗

PubMed2026

Fatty acids and breast cancer: Epidemiology, subtype-specific metabolism, immune regulation, and clinical translation.

Fatty acids (FAs) are bioactive dietary and metabolic molecules that participate in membrane architecture, energy homeostasis, inflammatory signaling, gene regulation and immune function, all of which intersect with breast cancer (BC) risk, progression and treatment response. In this narrative review we integrate epidemiological, clinical, translational and mechanistic evidence on the role of FAs in BC. Saturated, monounsaturated, trans- and polyunsaturated FAs (PUFAs) are treated as distinct biological exposures rather than interchangeable measures of total fat intake. Similarly, evidence from dietary assessment, circulating biomarkers, erythrocyte membrane composition, adipose tissue stores and tumor lipid signatures is interpreted separately, because each captures exposure and biology at a different level. BC subtypes differ in FA synthesis, uptake, oxidation, storage and remodeling: luminal tumors are frequently linked to hormone-regulated lipogenesis, human epidermal growth factor receptor 2 (HER2)-positive tumors to growth-factor-driven lipid metabolism, and triple-negative tumors to exogenous FA uptake, inflammatory lipid mediators and ferroptosis-related vulnerabilities. FA-derived mediators also shape immune-cell polarization, cytokine signaling and the tumor microenvironment, and dietary FAs may reshape the gut microbiota; the fiber-derived short-chain FAs it produces, distinct from dietary FAs, likewise help regulate immune and inflammatory tone. Clinical data suggest possible roles for fat-quality modification and selected n-3 PUFA interventions, but findings are heterogeneous and not yet sufficient to support routine biomarker-guided precision onco-nutrition. Candidate biomarkers, such as erythrocyte n-6:n-3 composition, require prospective validation before clinical implementation. FA biology thus represents a modifiable but complex axis in BC prevention, tumor biology and supportive care.

Humans↗

PubMed2026

Genomic analyses implicate hormonal and metabolic dysregulation in polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) and its underlying features remain poorly understood. In this genetic study (n = 544,513), we expand the number of genetic loci from 16 to 29, and additionally identify 31 associated plasma proteins. Many risk-increasing loci were associated with later age at menopause, underscoring the reproductive longevity related to an increased oocyte number and/or availability across the lifespan. Hormonal regulation in the etiology of this condition, through metabolic and reproductive features, was emphasized. The proteomic analysis highlighted metabolic biology known to be related to PCOS. A polygenic risk score (PRS) was associated with adverse cardiometabolic outcomes, with differing relevance of testosterone and body mass index in women and men. Finally, while oligo-anovulation and anovulatory infertility are features of PCOS, we observed no impact of PCOS susceptibility on childlessness. We suggest that PCOS susceptibility confers balanced pleiotropic influences on fertility in women, and life-long adverse metabolic consequences in both sexes.

Humans↗

PubMed2026

Plant-derived and microbial biostimulants in sustainable agriculture: mechanisms, applications, and challenges.

Plant biostimulants have emerged as transformative and sustainable tools for improving crop productivity, resource-use efficiency, and resilience under rapidly intensifying environmental stresses. Unlike conventional agrochemicals, biostimulants function by activating physiological, biochemical, and molecular processes that optimize plant performance without directly supplying nutrients or exerting pesticidal effects. This review comprehensively examines the integrated roles of plant-derived and microbial biostimulants in sustainable agriculture, with particular emphasis on microbial-mediated mechanisms underlying plant stress adaptation and rhizosphere functioning. Plant-derived biostimulants, including seaweed extracts, humic substances, protein hydrolysates, amino acids, and chitosan, enhance nutrient acquisition, root architecture, hormonal regulation, and antioxidant defense systems. More importantly, microbial biostimulants, such as plant growth-promoting rhizobacteria (PGPR), endophytic microorganisms, mycorrhizal fungi, actinomycetes, yeasts, and cyanobacteria, exert multifunctional effects through biological nitrogen fixation, mineral solubilization, phytohormone biosynthesis, volatile signaling, osmolyte accumulation, pathogen suppression, and modulation of stress-responsive genes. These beneficial microorganisms reshape rhizosphere microbial communities, improve nutrient cycling, and enhance plant tolerance to drought, salinity, heat, and heavy metal toxicity. Emerging evidence from genomics, transcriptomics, metabolomics, and microbiome-based investigations has further revealed the molecular networks and signaling pathways governing biostimulant-induced resilience and plant-microbe interactions. Despite their substantial promise, inconsistent field performance, formulation instability, regulatory limitations, and inadequate mechanistic understanding continue to restrict their large-scale adoption. This review highlights recent advances in microbial and plant-derived biostimulants while identifying critical knowledge gaps and future opportunities for precision biostimulant engineering, microbiome manipulation, and climate-resilient crop management. The integration of next generation biostimulant technologies into sustainable agricultural systems may significantly reduce dependence on agrochemicals while improving crop productivity, environmental sustainability, and global food security.

Agriculture↗

PubMed2026

Comparative genomics and full-length transcriptome profiling of wing morphs in Tetrix grossus (Orthoptera: Tetrigidae).

Wing polymorphism represents a paradigmatic dispersal-reproduction trade-off, yet its molecular basis remains uncharacterised in the phylogenetically distant pygmy grasshoppers (Tetrigidae). Here we integrate comparative genomics across ten orthopteran species with full-length transcriptomics of long-winged (FL) and short-winged (FS) Tetrix grossus. OrthoFinder recovered 118 orthogroups specific to T. grossus. Against a backdrop of pronounced gene-family contraction (36 expansions versus 222 contractions; net -186, mirrored at the ancestral Tetrix node, +37/-140), we identified an ancestral, Tetrix-specific expansion of hormone-regulation (12 genes; fold enrichment 7.93) and lipid/carbohydrate-metabolic families organised into syntenic clusters, alongside 513 positively selected genes enriched for integrin-mediated cell adhesion (6 genes), a process relevant to epithelial and appendage morphogenesis. Full-length transcriptomics of one long-winged (FL) and one short-winged (FS) adult female detected 7530 (FL) and 7515 (FS) expressed genes, with 794 FL- and 776 FS-restricted transcriptome-derived SNP-associated genes. The FL morph was enriched for an EGFR/Ras-Rho developmental-patterning axis and neuromuscular flight genes, whereas the FS morph was enriched for insulin/peptide-hormone response and growth-regulatory loci. Overall, we present genomic resources and testable hypotheses concerning the evolution and regulation of wing morphs in Tetrigidae rather than a validated genetic architecture of wing-morph determination.

Animals↗

PubMed2026

Genome-wide association and selective sweep analyses reveal genetic loci for teat number trait in pigs.

Teat number is a key reproductive trait for the commercial pig industry, as an optimum number enhances weaned piglet survival rate. This study aimed to identify single nucleotide polymorphisms (SNPs) and genomic regions that are associated with teat number in the Large White sow. A total of 1000 French Large White sows were used in an analysis of total, left/right, and maximum unilateral teat number. Environmental factor, Spearman correlation, genome-wide association study (GWAS), linkage disequilibrium, and selective sweep analyses were conducted, with validation performed in a population of 1145 Landrace pigs. Genetic statistics showed that this population's teat number had moderate-low genomic heritability (h2 = 0.17-0.21) and weak negative correlation with weaned piglet litter weight. Parity and season affected teat development. GWAS identified 17 candidate SNPs on SSC 4, 7, and 17. Combined with selective sweep analysis, two key regions on SSC 7 were found, with four teat number-related SNPs, annotated to VRTN, DIO2, NRXN3. These candidate genes are associated with thoracic vertebrae development, hormone regulation during the early stage of teat formation, and nervous system development. These five SNPs showed similar results in the Landrace pig validation population; non-mutant homozygotes had 0.25-1.15 more teats than mutant ones in both populations. This study contributes to the identification of key variant loci associated with teat number-related traits in sows, thereby providing reliable molecular markers and a theoretical basis for marker-assisted selection of sow reproductive performance.

Animals↗

PubMed2026

Meta-ERS: an exposome-based risk score using non-genetic factors to guide osteoporosis prevention.

BACKGROUND: Osteoporosis is influenced by both genetic and environmental factors, yet the relative contribution of the exposome remains unclear. This study aimed to systematically identify non-genetic exposures related to osteoporosis and develop an exposome risk score (ERS) to evaluate individual osteoporosis susceptibility. METHODS: We conducted an exposome-wide analysis of 477,792 UK Biobank participants to identify key exposures associated with osteoporosis. The selected exposures were combined into a weighted Meta-ERS and validated in the Scotland/Wales cohort. The Meta-ERS was further compared with polygenic risk scores (PRS) and linked to plasma proteomics to explore underlying biological pathways. RESULTS: We identified 41 independent non-genetic exposures spanning socioeconomic status, mental health, sleep, diet, smoking, physical activity, environment, and marital status, with socioeconomic status and mental health emerging as the most significant drivers. Based on the identified exposures, we constructed eight domain-specific exposure risk scores and integrated them into a weighted Meta-ERS. The Meta-ERS (R2 = 5.1%; Proportion of Chi-Square = 14.3%) demonstrated an ability to explain osteoporosis variation that was on par with polygenic risk scores (R2 = 4.8%; Proportion of Chi-Square = 12.0%). Importantly, modifying unfavorable exposures mitigated the negative effect of PRS on osteoporosis, particularly among high PRS individuals (1.5- to 1.8-fold greater absolute risk reduction than in those with low PRS). Proteomic analyses further revealed potential mechanisms through which the exposome influences osteoporosis, including hormonal regulation, inflammation, ossification, muscle development, lipid metabolism, and accelerated bone aging. Among these, growth/differentiation factor 15 was identified as a key mediator protein, with a mediation proportion of 13.13%-36.52%. CONCLUSIONS: The Meta-ERS facilitates the quantification of individual osteoporosis risk and identifies modifiable exposures for targeted prevention. Its application can enable personalized risk stratification and guide lifestyle or environmental interventions.

Aged↗

PubMed2024

Relaxin Modulates the Genomic Actions and Biological Effects of Estrogen in the Myometrium.

Estradiol (E2) and relaxin (Rln) are steroid and polypeptide hormones, respectively, with important roles in the female reproductive tract, including myometrium. Some actions of Rln, which are mediated by its membrane receptor RXFP1, require or are augmented by E2 signaling through its cognate nuclear steroid receptor, estrogen receptor alpha (ERα). In contrast, other actions of Rln act in opposition to the effects of E2. Here we explored the molecular and genomic mechanisms that underlie the functional interplay between E2 and Rln in the myometrium. We used both ovariectomized female mice and immortalized human myometrial cells expressing wild-type or mutant ERα (hTERT-HM-ERα cells). Our results indicate that Rln modulates the genomic actions and biological effects of estrogen in the myometrium and myometrial cells by reducing phosphorylation of ERα on serine 118 (S118), as well as by reducing the E2-dependent binding of ERα across the genome. These effects were associated with changes in the hormone-regulated transcriptome, including a decrease in the E2-dependent expression of some genes and enhanced expression of others. The inhibitory effects of Rln cotreatment on the E2-dependent phosphorylation of ERα required the nuclear dual-specificity phosphatases DUSP1 and DUSP5. Moreover, the inhibitory effects of Rln were reflected in a concomitant inhibition of the E2-dependent contraction of myometrial cells. Collectively, our results identify a pathway that integrates Rln/RXFP1 and E2/ERα signaling, resulting in a convergence of membrane and nuclear signaling pathways to control genomic and biological outcomes.

Female↗

PubMed2026

Arrhythmia and cardiomyopathy risk in Taiwan with complementary biobank evidence on thyroid genetic susceptibility: an integrative population-based framework.

BACKGROUND: Arrhythmia-induced cardiomyopathy (AiCM) is a potentially reversible cause of ventricular dysfunction; however, only a subset of patients with arrhythmia develop cardiomyopathy. Emerging evidence suggests that endocrine factors, particularly thyroid dysfunction with genetic susceptibility, may contribute to inter-individual variability in arrhythmia-related myocardial outcomes. METHODS: We performed a dual-cohort population-based study using the National Health Insurance Research Database (NHIRD, 2000-2015) and the Taiwan Biobank (TWB). In NHIRD, we examined the association between newly diagnosed arrhythmia and incident cardiomyopathy using Cox proportional hazards models. In TWB, genome-wide data, thyroid-stimulating hormone (TSH), polygenic risk scores (PRSs), lifestyle factors, and metabolic comorbidities were analyzed using multivariable regression and interaction models to assess determinants of thyroid dysfunction. RESULTS: In the NHIRD cohort, arrhythmia was associated with a significantly increased risk of incident cardiomyopathy (adjusted hazard ratio (aHR): 2.49, 95% CI: 1.94-2.96), with atrial fibrillation showing the strongest association among arrhythmia subtypes. In the TWB cohort, a higher thyroid polygenic risk score was strongly associated with thyroid dysfunction (adjusted odds ratio (aOR): 6.64, 95% CI: 5.86-7.52). The association between genetic susceptibility and thyroid dysfunction was further modified by metabolic and lifestyle factors, including diabetes, hyperlipidemia, and dietary patterns. Genome-wide analysis identified multiple loci associated with thyroid-stimulating hormone regulation, consistent with a polygenic architecture of thyroid endocrine traits. CONCLUSION: Arrhythmia was associated with an increased risk of cardiomyopathy in a nationwide cohort, while thyroid genetic susceptibility was strongly associated with thyroid dysfunction in a biobank cohort and modified by metabolic and lifestyle factors. These findings provide complementary population-level evidence of parallel cardiovascular and endocrine-genetic associations. Because the two cohorts were not individually linked, causal inference cannot be established. The results support a systems-level framework of endocrine-cardiac interaction and suggest that integrated clinical and genetic risk assessment may help identify individuals who warrant closer monitoring.

arrhythmia↗

PubMed2026

An overview of the DNA damage response in female reproductive system and breast cancers: A narrative review.

The DNA damage response (DDR) is a fundamental cellular network that preserves genomic integrity, and its dysregulation drives initiation, progression, and therapeutic response in female reproductive system and breast cancers. This narrative review provides a comparative analysis of DDR alterations across ovarian, endometrial, cervical, and breast cancers, synthesizing molecular studies, clinical trials, and international guidelines from PubMed/MEDLINE, Scopus, and Web of Science. DDR alterations vary substantially among these cancers, reflecting differences in tissue origin, hormonal regulation, and viral oncogenesis. Homologous recombination repair defects, particularly in breast cancer susceptibility 1/2, partner and localizer of BRCA2, ataxia telangiectasia mutated, and checkpoint kinase 2), are prevalent in ovarian, endometrial, and breast cancers, predicting sensitivity to platinum-based chemotherapy and poly (ADP-ribose) polymerase inhibitors. In endometrial cancer, homologous recombination deficiency predominates in high-grade tumor protein p53-mutated subtypes, while Fanconi anemia pathway alterations characterize aggressive serous carcinomas. Cervical cancer exhibits virus-induced DDR disruption and replication stress. Quantitative biomarkers, including tumor mutational burden, microsatellite instability, Radiation sensitive 51, Fanconi anemia complementation group D2, excision repair cross-complementation group 1, and DDR-related microRNAs enable patient stratification. Emerging ataxia telangiectasia and Rad3-related and WEE1 inhibitors show promise in combination regimens. Understanding of tumor-specific DDR enables rational therapeutic stratification, providing a framework for precision oncology.

DNA damage response, Ovarian neoplasms, Endometria↗

PubMed2026

Molecular and transcriptional regulation of plant defense responses to aphid infestation.

Aphids are one of the important agricultural pests causing substantial yield losses in crops grown across the globe. Aphids are known to cause direct feeding damages and indirect losses due to sooty mold development and plant virus transmission. Plants respond to these attacks by mounting a complex defense response at the infested sites and systemic levels. This multilayered defense response involves a highly coordinated network of phytohormones and other signalling components like Ca2+, mitogen activated protein kinases and reactive oxygen species. Key to these complex responses is a well-regulated gene expression involving several transcription factors. A wide range of transcription factors are structurally and functionally characterized across some model plants and in a few agronomically important crops. These transcription factors play diverse roles such as defense gene expression modulation, regulation of hormone signaling, secondary metabolism, oxidative stress response, cell wall modifications, and phloem-based defense. Understanding the integration of signaling pathways, hormone crosstalk, and transcription factor mediated regulation provides a framework for practical applications, including breeding, genome editing, and elicitor-based strategies. This review highlights how plant defense signaling and transcriptional regulation against aphids can be harnessed to develop sustainable and novel pest management solutions.

Aphid↗