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PubMed2026

Fetal hypoxia causes oocyte oxidative stress damage via the Sirt3/Sod2 pathway and can be alleviated by nicotinamide mononucleotide.

Environmental hypoxia exerts detrimental effects on the reproductive capabilities of both humans and animals. A fetal hypoxia model was established in which fetal mice were kept in a high-plateau hypoxic setting from embryonic day (E) 0 to 16.5. In our previous research, we found that fetal hypoxia exposure perturbs the methylation of imprinted genes in adult sperm and causes intergenerational placental impairments in male offspring. However, the specific impacts of fetal hypoxia on the female reproductive system, particularly regarding oocyte maturation, remain poorly understood. First, we found that fetal hypoxia mice exhibited a significant reduction in the average number of pups per litter. We conducted a comprehensive analysis of the transcriptome in oocytes from the hypoxic group and investigated the metabolic alterations within the follicular microenvironment. Fetal hypoxic stress contributed to cleavage and blastocyst rate reduction and induced early apoptosis and DNA damage triggered by mitochondrial dysfunction, oxidative stress aggravation and Sirt3/Sod2 downregulation. Additionally, administration of nicotinamide mononucleotide (NMN) has been shown to prevent oocytes from mitochondrial dysfunction and developmental impairment by increasing the expression of Sirt3/Sod2 and autophagy. The number of pups per litter in fetal hypoxia mice was reduced by 57.7% compared to the control group, while NMN intervention could restore it to 73.1% of the control group. These results indicate that fetal hypoxia exposure exerts multiple potential damages to adult female reproduction, while highlighting the clinical potential of NMN supplementation as a targeted intervention to alleviate such hypoxia-associated female reproductive impairment.

Animals↗

PubMed2026

Analysis of tuberculosis and multiple diseases as co-morbidities: a narrative review.

BACKGROUND: Tuberculosis (TB) remains the leading cause of death from infectious diseases worldwide, and its control is increasingly complicated by chronic comorbidities. Diabetes mellitus (DM), human immunodeficiency virus (HIV) infection, chronic obstructive pulmonary disease (COPD), and lung cancer (LC) substantially affect TB susceptibility, diagnosis, treatment, and prognosis. METHODS: This narrative review summarizes evidence on the interactions between TB and DM, HIV infection, COPD, and LC. Relevant literature was identified through PubMed, Web of Science, and World Health Organization publications, focusing on studies published between 2001 and 2025. Priority was given to peer-reviewed original studies and reviews addressing immune mechanisms, diagnosis, and treatment. RESULTS: DM increases TB risk by impairing innate and adaptive immunity and complicates prevention, diagnosis, and treatment. HIV-1 weakens antimycobacterial defense through lymphocyte depletion, macrophage dysfunction, granuloma instability, and immune exhaustion, markedly increasing susceptibility to active TB. TB and COPD mutually aggravate pulmonary inflammation, oxidative stress, and structural lung damage, contributing to poor respiratory outcomes. Mycobacterium tuberculosis(M.tb) infection may also be associated with LC development through chronic inflammation, oxidative stress-related genomic instability, and oncogenic signaling. Overall, these comorbidities increase diagnostic difficulty, therapeutic complexity, and the risk of adverse outcomes. CONCLUSIONS: TB associated comorbidities remain a major challenge to global TB control. Understanding these interactions may support bidirectional screening, risk stratification, and integrated management. Although these conditions share immune dysregulation, chronic inflammation, and oxidative stress, they differ in dominant mechanisms, diagnostic challenges, and treatment priorities. Future research should prioritize biomarker discovery, mechanistic clarification, and multilevel prevention and control strategies.

Humans↗

PubMed2026

Calcium-Sensing Receptor Activation Disrupts Phosphatidylserine Asymmetry and Promotes Calcium Oxalate Crystal-Induced Epithelial Injury in Renal Tubular Epithelial Cells.

BACKGROUND: Calcium oxalate (CaOx) crystal retention on the renal tubular epithelium is a key step in urolithiasis. Phosphatidylserine (PS) exposure may facilitate crystal-cell adhesion, but the upstream signaling mechanisms and the relative contributions of impaired inward PS flipping versus outward PS redistribution remain unclear. MATERIALS AND METHODS: Global proteomic profiling using 2-dimensional electrophoresis and matrix-assisted laser desorption/ionization time-of-flight/time-of-flight mass spectrometry (2-DE/MALDI-TOF/TOF) in an immortalized human proximal tubular epithelial cell line (HK-2) cells exposed to calcium oxalate monohydrate (COM) identified upregulation of the calcium-sensing receptor (CaSR). HK-2 cells were treated with COM with or without the CaSR antagonist NPS2390 or the CaSR agonist gadolinium chloride (GdCl3). Bidirectional PS transport was assessed using an N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl) (NBD)-labeled phosphatidylserine (NBD-PS) fluorescence-quenching assay, and surface PS exposure was measured by annexin V binding. Aminophospholipid translocase (APLT) expression, APLT-dependent inward PS transport, crystal adhesion, oxidative stress, and apoptosis-related signaling were evaluated. RESULTS: COM increased CaSR expression, enhanced surface PS exposure, and promoted crystal adhesion with concurrent oxidative stress and apoptosis-related signaling. COM induced a CaSR-sensitive defect in APLT-dependent inward PS flipping: NPS2390 partially restored inward PS transport and APLT expression, whereas GdCl3 exacerbated these changes. In contrast, COM-enhanced outward PS redistribution and externalization was largely unaffected by CaSR modulation, indicating relative CaSR insensitivity of the outward process. Consistently, CaSR activation aggravated, while CaSR inhibition attenuated, crystal adhesion and injury-related readouts. CONCLUSIONS: COM was associated with enhanced crystal-cell adhesion, CaSR activation, and a CaSR-sensitive impairment of APLT-dependent inward PS flipping, whereas enhanced outward PS redistribution appeared largely CaSR-insensitive. Pharmacologic inhibition of CaSR attenuated epithelial injury and crystal retention-related readouts, suggesting that CaSR may represent a potential therapeutic target.

Receptors, Calcium-Sensing↗

PubMed1976

[Usefulness of fat infusion within the frame of parenteral feeding].

The interactions of fat and carbohydrate metabolism are surveyed. The posttraumatic metabolism is characterized by a stress induced high lipolytic rate and a high concentration of non-esterified fatty acids in the blood. The increased fatty acid oxidation causes by effects of metabolites a catabolic situation with enhanced ketogenesis, gluconeogenesis and protein breakdown. High levels of fatty acids and ketone bodies reduce peripheral glucose utilization. In such a situation, infusions of fat emulsions are disadvantageous, since fatty acids, set free from the triglycerides, would aggravate the catabolic metabolism and change the nitrogen balance for the worse. In normal metabolic situations with high energy need, or in long term parenteral nutrition, fat infusions are necessary to meet the needs of energy and of essential fatty acids. Fat infusions shoudl be combined with carbohydrates and amino acids in an appropriate relation.

Amino Acids↗

PubMed1979

The possible role of hypertension in aggravating hemolytic episodes in G-6PD deficient persons.

Approximately 13 percent of American Negro males carry a mutant [A-variant] glucose-6-phosphate dehydrogenase enzyme in their red blood cells that predisposes them to hemolytic episodes following exposure to oxidant drugs such as primaquine. Most hemolytic episodes to standard prophylactic treatment are mild and self-limited, but as many as 2 percent of Negro males develop severe hemolysis when similarly treated. The exaggerated response may be due in part to the combination of G-6-PD deficiency and hypertension since hypertension can cause red cell fragmentation, and the stressed cells of G-6-PD deficient person would be more sensitive to such fragmentation.

Anemia, Hemolytic, Congenital↗

PubMed2025

Therapeutic Targeting of Decr1 Ameliorates Cardiomyopathy by Suppressing Mitochondrial Fatty Acid Oxidation in Diabetic Mice.

BACKGROUND: A significant increase in mitochondrial fatty acid oxidation (FAO) is now increasingly recognized as one of the metabolic alterations in diabetic cardiomyopathy (DCM). However, the molecular mechanisms underlying mitochondrial FAO impairment in DCM remain to be fully elucidated. METHODS: A type 2 diabetes (T2D) mouse model was established by a combination of high-fat diet (HFD) and streptozotocin (STZ) injection. Neonatal rat cardiomyocytes were treated with high glucose (HG) and palmitic acid (HP) to simulate diabetic cardiac injury. Gain- and loss-of-function approaches and RNA sequencing were utilized to investigate the role and mechanism of 2,4-dienoyl-CoA reductase 1 (Decr1) in DCM. RESULTS: By integrating the genomic data available in the Gene Expression Omnibus (GEO) with DCM rodents, we found that the transcriptional level of Decr1 was consistently upregulated in DCM (+255% for diabetic heart, p < 0.0001; +281% for diabetic cells, p < 0.0001). Cardiomyocytes-specific knockdown of Decr1 preserved cardiac function (+41% for EF, p < 0.0001; +24% for FS, p = 0.0052), inhibited cardiac hypertrophy (-34%, p < 0.0001), fibrosis (-69%, p < 0.0001), apoptosis (-56%, p < 0.0001) and oxidative damage (-59%, p < 0.0001) in DCM mice, while cardiomyocytes-specific overexpression of Decr1 aggravated DCM (-28% for EF, p = 0.0347; -17% for FS, p = 0.0014). Deletion of Decr1 prevented high glucose/palmitate (HG/HP)-induced hypertrophy (-22%, p = 0.0006), mitochondrial dysfunction and apoptosis (-74%, p < 0.0001) in cultured cardiomyocytes. Furthermore, RNA sequencing and functional analysis showed that Decr1 interacted with and upregulated pyruvate dehydrogenase kinase 4 (PDK4) in injured cardiomyocytes, and overexpression of PDK4 eliminated the benefits of Decr1 downregulation in DCM (-20% for EF, p = 0.0071; -28% for FS, p = 0.0022). Mechanistically, PDK4 acted as a kinase that induced phosphorylation and mitochondrial translocation of HDAC3. In the mitochondria, HDAC3 mediated the deacetylation of dehydrogenase trifunctional multienzyme complex α subunit (HADHA), contributing to excessive mitochondrial FAO and subsequent cardiac injury. From a screening of 256 natural products, we identified Atranorin and Kurarinone as potential inhibitors of Decr1, both demonstrating protective effects against DCM (Atranorin, +21% for EF, p = 0.0134; +24% for FS, p = 0.0006; Kurarinone, +20% for EF, p = 0.0183; +27% for FS, p = 0.0001). CONCLUSIONS: Our study delineates a molecular mechanism by which Decr1 potentiated higher mitochondrial lipid oxidation and cardiac damage by enhancing HADHA deacetylation through the PDK4/HDAC3 signalling pathway.

Animals↗