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PubMed2026

Cis-regulatory evolution of CsANS1 drives cultivar variation in anthocyanin accumulation in tea plants.

Anthocyanins, a ubiquitous class of water-soluble phytochemicals renowned for their chromatic diversity and potent bioactivity, are integral to the phenotypic and metabolic plasticity of higher plants. Using an integrative multi-omics approach that combines transcriptomic and metabolomic profiling, we identified anthocyanin synthase (CsANS1) as the key genetic determinant responsible for interspecific variation in anthocyanin accumulation among tea plants. Architectural comparison of promoter regions revealed a 192-bp variation insertion in the CsANS1 cis-regulatory region with potential functional significance. This insertion was strictly conserved in anthocyanin-rich (purple-leaf) cultivars, including both natural and hybrid genotypes, but entirely missing in anthocyanin-deficient (green-leaf) cultivars. Dual-luciferase assays confirmed that this insertion enhances promoter activity. Additionally, we delineated a tripartite regulatory axis comprising CsmiR156b, CsSPL9, and CsMYB75 which orchestrates the spatiotemporal modulation of CsANS1 expression and, consequently, anthocyanin biosynthesis. Collectively, these findings provide a mechanistic paradigm for anthocyanin polymorphism in tea plants, implicating both cis-regulatory evolution and transcriptional network synergy as pivotal drivers of phytochemical diversification.

Anthocyanins↗

PubMed2025

Aplf/Dna2 variants drive chromosomal fission and accelerate speciation in zokors.

Chromosomal fissions and fusions are common, yet the molecular mechanisms and implications in speciation remain poorly understood. Here, we confirm a fission event in one zokor species through multiple-omics and functional analyses. We traced this event to a mutation in a splicing enhancer of the DNA repair gene Aplf in the fission-bearing species, which caused exon skipping and produced a truncated protein that disrupted DNA repair. An intronic deletion in Dna2, known to facilitate neo-telomere formation when knocked out, reduced gene activity. These variants collectively drove chromosomal fission in this zokor species. The newly formed chromosome became fixed due to carrying essential genes and strong selective pressure. While geographic isolation likely initiated the divergence of this species and the sister one, the fission event and associated decline at the chromosome level in gene flow probably exacerbated the speciation process. Our work elucidates the genetic basis of chromosomal fission and underscores its role in speciation dynamics.

Multiomics↗

PubMed2026

Longitudinal dynamics of gene expression and metabolomics in an aging population cohort.

Multiomic profiling provides a comprehensive physiological overview at the molecular level, but understanding of its spatiotemporal dynamics remains limited in human populations. We profiled longitudinal whole-blood gene expression and metabolite levels in 335 females over 8 years. Levels of 5061 genes and 181 metabolites changed over time, with individual trajectories often diverging from population-level trends. Longitudinally variable genes showed cell type specificity and enrichment for aging-relevant pathways, including cardiometabolic and neurodegenerative disorders. Longitudinal trajectories were further shaped by genetics, circadian rhythm, seasonality, and environmental pollutant exposures. Integrative analyses revealed extensive static and time-variable cross-omic connectivity. Longitudinal profiling offers insight into the temporal evolution of age-related conditions at the molecular level, and understanding individual variation within these longitudinal patterns will be essential for future precision medicine approaches.

Female↗

PubMed2026

SpxA1 and SpxA2 function as a stoichiometry-dependent regulatory rheostat governing virulence gene expression in group A Streptococcus.

UNLABELLED: Group A Streptococcus (GAS) is a human-restricted pathogen whose global incidence has surged in the post-COVID era. The ability of GAS to shift from a colonizing to invasive phenotype depends on coordinated virulence gene regulation in response to host-derived signals. However, the mechanisms by which individual stress-sensing systems interact to reshape the virulence gene regulatory landscape remain incompletely understood. Here, we define the regulatory programs of two conserved transcriptional regulator paralogs, SpxA1 and SpxA2, using an integrated multi-omic approach combining RNA-seq, data-independent acquisition proteomics, NanoString-based transcriptional profiling across multiple host-relevant stress conditions, and chromatin immunoprecipitation with exonuclease treatment (ChIP-exo). RNA-seq revealed functionally distinct regulons with SpxA1 governing oxidative stress defense and SpxA2 coordinating virulence-associated gene expression linked to the CovRS two-component regulatory system. Proteomic analysis established SpxA2 as a ClpXP protease substrate in GAS and identified reciprocal paralog accumulation upon loss of either SpxA1 or SpxA2, consistent with compensatory transcriptional upregulation. NanoString profiling under bacitracin and human neutrophil peptide-1 challenge identified four gene modules with distinct stoichiometry-dependent and condition-dependent regulatory logic, revealing that the SpxA1/SpxA2 ratio rather than the activity of either paralog alone determines which transcriptional programs are engaged. ChIP-exo demonstrated that SpxA2 directly modulates CovR-DNA binding occupancy in a CovR-binding motif-dependent manner, simultaneously antagonizing CovR dimer binding at an extended (25 bp) CovR motif and facilitating CovR monomer binding at the canonical ATTARA motif. These findings establish the LiaFSR-SpxA2-CovRS axis as a cross-regulatory circuit through which GAS cell envelope stress sensing is directly transduced into coordinated virulence gene regulatory changes. IMPORTANCE: Group A Streptococcus (GAS) causes millions of infections annually, including a recent global surge in invasive disease. To survive in the human host, GAS must rapidly reprogram virulence gene expression in response to host-derived stresses. This study characterizes two conserved transcriptional regulators, SpxA1 and SpxA2, that govern this response through interaction with RNA polymerase to indirectly influence the DNA-binding activity of downstream transcription factors. We show that SpxA2, activated by a cell envelope stress-sensing system responding to human antimicrobial peptides, reshapes the binding of the master virulence regulator CovR in a promoter-specific manner, coupling cell envelope stress sensing to virulence gene regulation. The stoichiometric balance between SpxA1 and SpxA2 functions as a regulatory rheostat calibrating overall virulence gene regulatory tone, providing a framework for understanding how RNA polymerase-interacting regulators coordinate stress responses and virulence gene control across Gram-positive bacterial pathogens.

Streptococcus pyogenes↗

PubMed2026

Phytohormones in fungi: inter-kingdom modulators or fungal self-controlling elements?

SUMMARYLeveraging data from innovative experimental approaches, omics technologies, and bioinformatics, we offer new insights into how fungi communicate with and perceive their environment to achieve ecological success. By integrating comparative data from both the fungal and plant kingdoms, we critically reassessed the evolutionary, biochemical, and functional landscape of phytohormones in fungi, challenging the conventional notion that these molecules serve exclusively as plant regulators or as means of communication with them. Our analysis demonstrates that fungi not only synthesize a diverse array of phytohormones-including auxins, cytokinins, gibberellins, abscisic acid, ethylene, brassinosteroids, salicylic acid, and oxylipins-but also possess hormone-sensing and signal transduction mechanisms architecturally distinct from those of plants. Employing genomics, phylogenetics, and structural analyses, the review uncovers that many hormone biosynthetic and sensing pathways in fungi are evolutionarily ancient, sometimes predating their roles in plant-fungus interactions, and that some pathways show convergence rather than direct gene homology. Fungal phytohormones regulate development, growth, and metabolism, thereby playing key functions in their ecological context. The review emphasizes that, while biosynthetic pathways tend to be highly conserved, perception and signaling mechanisms in fungi are more varied and often remain poorly understood. We conclude that fungi have an intrinsic and autonomous hormonal physiology that underpins their ecological adaptability and success. Collectively, this analysis reframes fungal biology, highlighting the need for deeper investigation into the signaling and regulatory roles of phytohormones in fungi beyond their interactions with plants.

cell signaling↗

PubMed2026

Probiogenomic analysis of functional potential and safety of L. plantarum 8p-a3 and DMC-S1 strains: in silico vs in vitro and in vivo data.

The molecular basis of the beneficial effects and the causes of the negative effects of probiotics are not entirely clear. Clarifying these issues is important for understanding the biology and assessing the safety of the microbes. Omics technologies have opened up new resources for obtaining relevant knowledge. Here, for the first time, we present the results of a comparative analysis of the functional potential and safety of two L. plantarum strains: the approved probiotic 8p-a3 and the Drosophila intestinal resident, which exhibit opposite effects on D. melanogaster as the model host organism. Through genomic analysis, extracellular vesicle studies, and in vitro and in vivo assays, we have identified the common and specific characteristics of the strains. The strains proved to be similar in a set of genes that determine benefits to the host organism, as well as in the presence of some risk factors. Significant differences between the strains are related to genes responsible for adhesion, sialic acid metabolism, mucin degradation, antimicrobial peptides, tannin resistance, and immunomodulation. In silico data correlated with in vitro and in vivo data, with the exception of antimicrobial sensitivity. Pronounced differences between the strains were found in terms of the composition and biological effects of their vesicles. In vivo data on the effects of the strains correlate with the corresponding data of their vesicles in the fruit fly model. The results obtained open up new facets in L. plantarum strains relevant for evaluating the functionality and safety of probiotics.IMPORTANCEUsing a probiogenomic approach, common and specific features regarding functionality and safety were identified in the strains (the approved probiotic strain L. plantarum 8p-a3 and the Drosophila intestinal bacterium L. plantarum DMC-S1), which exhibit opposite effects on the model host organism (D. melanogaster). The genomic analysis was supplemented by the analysis of extracellular vesicles of the strains. Comparative analysis of in silico data in combination with in vitro and in vivo studies was performed, and unexpected capabilities of the strains were discovered. Novel factors, essential for evaluating the safety of probiotics, were identified. New facets in the interplay of probiotic bacterium with host organism have been revealed.

Animals↗

PubMed2026

Biocontrol effect of a solid-state fermentation-derived extract mixture of Trichoderma asperellum on sunflower Sclerotinia rot and associated host defense responses.

Sclerotinia disease is a destructive fungal disease of sunflowers, soybeans, and other economically important crops, causing substantial yield loss and quality deterioration. Long-term reliance on dose-dependent broad-spectrum fungicides is constrained by resistance risks and potential environmental burdens, creating tension with the sustainability goal of "reducing pesticide use while improving efficacy." Here, we explore a Trichoderma spp.-based microbial disease management strategy. Whole-genome sequencing of Trichoderma asperellum TCS007 isolated from Antarctic marine sediments, coupled with genome mining, predicted diverse biosynthetic gene clusters putatively associated with siderophores, polyketides, nonribosomal peptides, and terpenoids; the corresponding metabolites are not chemically confirmed and require further validation. Using a solid-state fermentation workflow, we prepared a fermentation-derived extract mixture (TCS007-SSF-Ex). In vitro assays showed dose-dependent inhibition of Sclerotinia sclerotiorum by TCS007-SSF-Ex (EC50 = 1.252 mg/L), and microscopy revealed cellular damage-consistent changes, including organelle disruption and plasmolysis. Pathogen transcriptomic and metabolism-related analyses indicated broad perturbations in organelle biogenesis and metabolic processes, with significant alterations in pathways associated with succinate, D-glucose, and phenylacetate; these results are consistent with growth inhibition and reduced pathogenicity, but specific molecular targets and causal links remain to be validated. In vivo, under certain application conditions, triple applications increased APX activity (+492.5%) and β-1,3-glucanase activity (+419.6%). Collectively, this work supports a "pathogen suppression-host defense induction" framework and facilitates subsequent identification of active components and mechanistic validation.IMPORTANCESclerotinia diseases cause recurrent and economically important losses in oilseed crops, while long-term fungicide use is constrained by resistance risks and environmental burdens. Trichoderma-based biocontrol is a promising complementary strategy, yet evidence supporting metabolite-containing Trichoderma-derived preparations as immune elicitors remains less consolidated than that for living inoculants, and scalable production routes are still needed. Here, we examine an Antarctic marine sediment-derived strain, Trichoderma asperellum TCS007, and a solid-state fermentation (SSF)-derived extract mixture (TCS007-SSF-Ex) produced via solid-state fermentation. We combine in vitro antifungal assays, pathogen ultrastructural observations, and correlative omics analyses with in vivo measurements of sunflower defense enzymes (APX and β-1,3-glucanase) to evaluate a "pathogen suppression-host defense induction" framework. Our findings support the potential of SSF-derived Trichoderma metabolite mixtures for greener management of Sclerotinia disease and provide a foundation for future chemical identification of active components and mechanistic validation.

Ascomycota↗

PubMed2026

Spatial habitat radiomics predicts tertiary lymphoid structure status and identifies an IDO1+ migratory dendritic cell axis in breast cancer.

BACKGROUND: Tertiary lymphoid structures (TLS) are spatially organized immune niches associated with therapeutic response and favorable outcomes in breast cancer (BC). However, TLS assessment currently relies on invasive tissue-based analyses, and the biological mechanisms underlying imaging-based TLS prediction remain poorly understood. METHODS: We developed and validated a spatial heterogeneity-based radiomic TLS signature (shTLS) using dynamic contrast-enhanced MRI to non-invasively predict TLS status across multicenter BC cohorts. Spatial habitat radiomics were used to capture intratumoral and peritumoral immune-related heterogeneity. Integrated multi-omics analyses, including transcriptomics, pathomics, genomics, single-cell RNA sequencing, immunohistochemistry, and multiplex immunofluorescence, were performed to biologically interpret shTLS-defined subgroups. Functional drug-sensitivity assays were conducted to assess therapeutic implications. RESULTS: The shTLS model achieved robust predictive performance across independent cohorts and molecular subtypes. High shTLS scores were associated with immune-inflamed tumors characterized by spatially clustered activated T cells and dendritic cells (DCs). In contrast, shTLS-low tumors exhibited an immunosuppressive spatial niche with peripheral accumulation of CD4+ PD-1+ T cells and plasma cells, increased immune-tumor separation, and enhanced inflammatory and immunoregulatory signaling. An indoleamine 2,3-dioxygenase 1 (IDO1)-associated immunoregulatory program was observed in the shTLS-low tumors, which appeared to be preferentially expressed by LAMP3+CCR7+ migratory DCs. Pharmacologic inhibition of IDO1 enhanced chemotherapy and CDK4/6 inhibitor sensitivity in vitro. CONCLUSION: This study establishes spatial radiomics as a non-invasive approach to decode TLS-associated immune ecosystems and supports the presence of an IDO1-associated immunosuppressive phenotype, providing biological insight and translational rationale for patient stratification and future combination strategies.

Humans↗

PubMed2026

Markers of microvascular instability predict severity and survival in idiopathic pulmonary fibrosis.

INTRODUCTION: Most research on idiopathic pulmonary fibrosis (IPF) has focused on the interplay among fibroblasts, the immune system and epithelial cells. There is growing evidence that microvascular dysfunction also plays a role in disease progression, but large human translational studies are lacking. In this research, we aim to identify a proteomic signature of microvascular instability and assess the impact of current therapeutics on the microvasculature. METHODS: Olink proteomic data from patients with IPF were obtained from the Pulmonary Fibrosis Foundation Patient Registry (PFF-PR) (n=914) and an independent validation cohort (n=366). Among the PFF-PR, 640 patients also have whole-blood RNA sequencing data available. A subset of 79 microvascular-associated proteins was curated, and their associations with disease severity and transplant-free survival were examined. An adaptive least absolute shrinkage and selection operator was used to generate a novel microvascular risk score. RESULTS: Higher plasma levels of five microvascular-associated proteins (SDC1, MMP10, THBS2, HGF and SERPINA5) were associated with lung function and survival in both cohorts. Whole-blood RNA sequencing of patients with microvascular risk revealed enrichment of immune-mediated processes. Patients with higher microvascular risk who were subsequently put on nintedanib in the following year had significantly better 3-year transplant-free survival compared with patients who did not receive antifibrotic intervention (HR 0.56, 95% CI 0.35 to 0.89, p=0.0142). DISCUSSION: Integrative multi-omics analyses suggest that perturbations to microvascular remodelling contribute to disease severity and progression in IPF. This analysis offers a framework for a precision medicine approach for IPF.

Idiopathic pulmonary fibrosis↗

PubMed2026

New Insights into Genomic Variations and Mutational Events Associated with Plant-Pathogen Interactions.

Plant diseases threaten global food security, causing up to 40% crop yield losses and more than $220 billion in annual economic damage. This review synthesizes recent advances in understanding the genomic variations and mutational events underlying plant-pathogen interactions and durable plant disease resistance. Key insights into evolutionary dynamics, genetic variability, and coadaptive strategies reveal the complexity of host-pathogen relationships and the implications for developing durable disease resistance. Integrative approaches combining genome-wide association studies and functional genomics have uncovered the polygenic and epistatic architecture of quantitative resistance. Advances in pan-genomics and high-throughput sequencing have revealed extensive genetic variability in cultivated/elite germplasm and wild relatives. Emerging technologies, including gene editing, multi-omics, and machine learning, enable predictive modeling of resistance traits and support evolution that informs plant breeding strategies. Collectively, these advances provide a robust framework for developing durable resistance and sustainable crop protection in the face of global agricultural challenges.

Host-Pathogen Interactions↗

PubMed2004

Proteomics.

The genome sequences of important model systems are available and the focus is now shifting to large-scale experiments enabled by this data. Following in the footsteps of genomics, we have functional genomics, proteomics, and even metabolomics, roughly paralleling the biological hierarchy of the transcription, translation, and production of small molecules. Proteomics is initially concerned with determining the structure, expression, localization, biochemical activity, interactions, and cellular roles of as many proteins as possible. There has been great progress owing to novel instrumentation, experimental strategies, and bioinformatics methods. The area of protein-protein interactions has been especially fruitful. First pass interaction maps of some model organisms exist, and the proteins in many important organelles are about to be determined. Researchers are also beginning to integrate large-scale data sets from various "omics" disciplines in targeted investigations of specific biomedical areas and in pursuit of a general framework for systems biology.

Genomics↗

PubMed2026

Novel association of NAV3 with dilated cardiomyopathy and its role in cardiac fibrosis.

A genome-wide association study (GWAS) identified neuron navigator 3 (NAV3) as a potential genetic determinant of myocardial recovery in dilated cardiomyopathy (DCM). This study aimed to understand its functional role in cardiac pathophysiology by leveraging omics approaches. Single-cell RNA-seq transcriptomic data from previously published adult human hearts indicate that NAV3 expression is highest in cardiac fibroblasts, suggesting its functional role in these cells. In vitro, stimulation of primary human ventricular cardiac fibroblasts with transforming growth factor β1 (TGF-β1) induced NAV3 expression in a dose and time-dependent manner. Small-interfering-RNA-mediated knockdown of NAV3 significantly attenuated TGF-β1-induced fibroblast activation, reducing the expression of α-smooth muscle actin (α-SMA), collagens, and fibronectin. RNA sequencing of NAV3-silenced fibroblasts, confirmed by Western blot, revealed upregulation of cell cycle regulators and downregulation of profibrotic markers, suggesting that NAV3 facilitates TGF-β1-induced cell cycle arrest and fibroblast-to-myofibroblast transition. Notably, NAV3 silencing did not alter canonical SMAD2/3 phosphorylation, implying a role for NAV3 in modulating fibrotic signaling through other pathways. Our findings provide functional and mechanistic insights into NAV3's novel role in cardiac fibrosis, showing that reduced NAV3 expression attenuates TGF-β1-mediated fibroblast activation by regulating cell cycle signaling. These results support further investigation of NAV3 as a potential modulator of cardiac fibrosis and myocardial recovery in DCM.NEW & NOTEWORTHY This study uncovers a previously unrecognized role for NAV3 in TGF-β1-driven cardiac fibroblast activation. We show that NAV3 facilitates profibrotic remodeling through noncanonical signaling and cell cycle arrest, independently of SMAD2/3. These findings position NAV3 as a novel regulator of fibroblast phenotype and a potential modulator of cardiac fibrosis.

Humans↗

PubMed2026

Drug repurposing using transcriptomics: principles and unmet needs in cardiovascular disease.

Although cardiovascular disease is the leading cause of death globally, therapeutic development in this field is slow. Given the high cost of developing new drugs and running clinical trials for cardiovascular disease, repurposing of drugs with approved safety profiles is an attractive strategy for therapeutic development that can significantly reduce the time and cost investment before phase II clinical trials. In the era of "Omics," various new methods and several large databases have been developed to enable the use of transcriptomics data for drug repurposing. This review summarizes the principles and workflow of signature mapping, which forms the foundation of statistical models used for transcriptome-based drug repurposing. We highlight the features of different analysis pipelines and databases that have been developed for signature mapping. These analysis pipelines prioritize genes that are statistically important, an approach that fundamentally differs from the pharmacological approach of identifying disease-driving and therapeutically targetable pathways. Outcomes of signature mapping pipelines are sensitive to the quality of input data, and results are not always reproducible. Moreover, all widely used RNA-seq databases are derived from cancer research and lack high-quality molecular data for cardiovascular disease. These unmet needs call for interdisciplinary collaboration and large networks of cardiovascular research-oriented biobanks to create the databases needed for transcriptomic-based signature mapping for drug repurposing efforts.

Drug Repositioning↗

PubMed2006

Population and systems genetics analyses of cortisol in pigs divergently selected for stress.

This study presents a systems genetic analysis on the physiology of cortisol in mice and pigs with an aim to show the potential of a comprehensive computational approach to quickly identify candidate genes and avoid a costly whole-genome quantitative trait locus (QTL) mapping. Population genetics analyses were performed on measurements of cortisol from a pig selection experiment. Expression QTL were mapped and gene networks were built using gene expressions for Crhr1 (corticotrophin-releasing hormone receptor) gene and single nucleotide polymorphisms from public mouse data. Results from mouse data were used to infer potential candidate regulatory genes involved in pig cortisol regulation, using a comparative or translational systems genetics approach. The pig data used were from a 10-yr divergent genetic selection experiment, providing data on 417 individuals. Population genetics analysis showed that cortisol is highly genetically determined with heritabilities of 0.40-0.70. Furthermore, a major gene with an additive effect of 86 ng/ml is segregating. Genetical-genomics investigations revealed two trans-acting eQTL for Crhr1 gene expression on chromosomes 2 and 13. Candidate gene search under trans-eQTL peaks yielded 63 genes for Crhr1 expression phenotypes. Functional links for Crhr1 genes with other genes/proteins in the gene network using mouse data were shown for the first 10 statistically significant genes involved. Results show translational or comparative systems genetics approaches reduce costs and time in large-scale genetics and "-omics" investigations. This is the first study to report a strong genetic basis for cortisol physiology using a systems approach.

Animals↗

PubMed2026

RAS-GTP Inhibition Overcomes Acquired Resistance to KRASG12C Inhibitors Mediated by Oncogenic and Wild-Type RAS Activation in Non-Small Cell Lung Cancer.

UNLABELLED: Small-molecule KRASG12C(OFF) inhibitors that bind to the inactive GDP-bound state of KRAS have demonstrated efficacy in patients with KRASG12C-mutant tumors, yet responses tend to be transient because of emergence of on-treatment resistance. Recently, RAS(ON) G12C-selective inhibitors, which bind to the active GTP-bound state of RAS, were described, and elironrasib is undergoing evaluation in multiple clinical trials. In this study, we generated resistant cell lines and patient-derived xenograft models to KRASG12C(OFF) and RAS(ON) G12C-selective inhibitors and interrogated resistance mechanisms using a multiomics strategy consisting of phosphoproteomics, whole-exome sequencing, and RNA sequencing combined with functional testing using small-molecule and CRISPR screens and RAS(ON) inhibitors being evaluated in clinical trials. Two models reactivated RAS signaling, either via KRASG12C gene amplification or NRASG13R mutation, and were vulnerable to dual inhibition by RAS(ON) G12C-selective and RAS(ON) multiselective inhibitors, RMC-4998 and RMC-7977. Two models, which lacked any discernable genomic alteration, acquired resistance associated with increased receptor tyrosine kinase activity and downstream persistent RAS activity and were sensitive to RAS-GTP inhibition by RMC-7977. Finally, one model displayed epithelial-mesenchymal transition, loss of RAS dependence, and acquired reliance on cell-cycle kinases and proteins associated with DNA damage response. This work highlights KRASG12C-selective inhibitor resistant states that parallel and complement clinical findings and demonstrate that a large subset could be overcome with a RAS(ON) multi-selective inhibitor as a stand-alone agent or in combination with other therapies. SIGNIFICANCE: Multi-omic characterization of resistance mechanisms to KRASG12C-selective inhibitors in non-small cell lung cancer provides insights that could inform precision medicine-based therapeutic approaches for improving the treatment of KRASG12C mutant tumors. See related article by Stern et al., p. 485.

Humans↗

PubMed2004

Proteomics in nephrology: current status and future directions.

Proteomics is one among various 'OMICS' fields that have been growing rapidly in the postgenomic era. During the past few years, proteomics has been extensively applied to several fields of medicine to better understand normal physiology, to define the pathophysiology of diseases, and to identify novel biomarkers and new therapeutic targets. This review focuses on current status and future directions of proteomics in the nephrology field. Recent studies of renal proteome, proteomes of individual intrarenal structures (i.e., glomerular, vascular, tubular, brush border membrane, mesangial, and podocyte proteomes), urinary proteome, and protein profiles in dialysate or ultrafiltrate removed by renal replacement therapy are summarized.

Animals↗

PubMed2026

State of Cardiovascular Disease and Stroke in Hispanic/Latino Adults in the United States: A Scientific Statement From the American Heart Association.

Cardiovascular disease became the leading cause of death among Hispanic individuals in the United States in 2022. Hispanic adults experience a disproportionate burden of cardiometabolic risk factors, including obesity, diabetes, and dyslipidemia. Hispanic populations are highly heterogeneous, with substantial variations in genetic ancestry and sociocultural influences that shape cardiovascular disease risk and outcomes. The "Hispanic paradox," describing lower cardiovascular disease mortality despite higher risk factor burden, is increasingly recognized as an oversimplification that does not apply uniformly across Hispanic heritage groups, sexes, or disease types. Disaggregated data reveal substantial differences in risk profiles and disease burden among Hispanic heritage groups, emphasizing the limitations of treating this population as a monolithic unit. Recent evidence demonstrates widening disparities in hypertension control, obesity, diabetes, and metabolic diseases among Hispanic populations, threatening this prior mortality advantage. Advancing cardiovascular and equitable health will require developing a deeper understanding of the unique drivers of cardiovascular disease within diverse Hispanic communities, addressing barriers such as language and insurance access, and implementing culturally tailored interventions and policies. This scientific statement summarizes current cardiovascular disease epidemiology in Hispanic populations, emphasizing heritage group variation and social and structural determinants of health, and presents strategies to improve prevention and healthcare delivery. Key priorities for advancing cardiovascular health in Hispanic adults include expanding disaggregated data collection, increasing representation in research, and ensuring equitable implementation of precision medicine approaches, including genomics, multi-omics, and artificial intelligence, while addressing environmental exposures, psychosocial stressors, and policy-related drivers of risk in order to achieve the American Heart Association's 2028 Impact Goals to advancing health and hope for everyone, everywhere.

AHA Scientific Statements↗

PubMed2024

Metagenomic Study of the MESA: Detection of Gemella Morbillorum and Association With Coronary Heart Disease.

BACKGROUND: Inflammation is a feature of coronary heart disease (CHD), but the role of proinflammatory microbial infection in CHD remains understudied. METHODS AND RESULTS: CHD was defined in the MESA (Multi-Ethnic Study of Atherosclerosis) as myocardial infarction (251 participants), resuscitated arrest (2 participants), and CHD death (80 participants). We analyzed sequencing reads from 4421 MESA participants in the National Heart, Lung, and Blood Institute Trans-Omics for Precision Medicine program using the PathSeq workflow of the Genome Analysis Tool Kit and a 65-gigabase microbial reference. Paired reads aligning to 840 microbes were detected in >1% of participants. The association of the presence of microbe reads with incident CHD (follow-up, ~18 years) was examined. First, important variables were ascertained using a single regularized Cox proportional hazard model, examining change of risk as a function of presence of microbe with age, sex, education level, Life's Simple 7, and inflammation. For variables of importance, the hazard ratio (HR) was estimated in separate (unregularized) Cox proportional hazard models including the same covariates (significance threshold Bonferroni corrected P<6×10-5, 0.05/840). Reads from 2 microbes were significantly associated with CHD: Gemella morbillorum (HR, 3.14 [95% CI, 1.92-5.12]; P=4.86×10-6) and Pseudomonas species NFACC19-2 (HR, 3.22 [95% CI, 2.03-5.41]; P=1.58×10-6). CONCLUSIONS: Metagenomics of whole-genome sequence reads opens a possible frontier for detection of pathogens for chronic diseases. The association of G morbillorum and Pseudomonas species reads with CHD raises the possibilities that microbes may drive atherosclerotic inflammation and that treatments for specific pathogens may provide clinical utility for CHD reduction.

Humans↗