Study on the mechanism of cardiomyocyte energy metabolism regulated by Echinocystic acid derivative in improving myocardial ischemia-reperfusion injury.

Exploration and validation of potential diagnostic biomarkers of PANoptosis in periodontitis using bioinformatics approaches.

Gami-Yukmijihwang-Tang ameliorates scopolamine-induced cognitive impairment by restoring cholinergic function and suppressing oxidative stress and neuroinflammation.

Compound Platycladus orientalis tincture promotes hair regrowth and is associated with hair-cycle progression and Wnt/β-catenin-related signaling.

Sleep disturbances, particularly obstructive sleep apnea (OSA) and sleep deprivation, are critical yet underrecognized contributors to male reproductive dysfunction. Both conditions disrupt endocrine homeostasis, reducing testosterone and luteinizing hormone levels, which are central regulators of spermatogenesis. This review aimed to synthesize current evidence on the mechanisms linking OSA and sleep deprivation to impaired male fertility, with emphasis on endocrine, oxidative, and inflammatory pathways. We conducted a structured, non-systematic narrative review using PubMed/MEDLINE, Scopus, and Web of Science databases, focusing on clinical and experimental studies evaluating the effects of sleep disturbances on male reproductive health. Disrupted sleep and OSA-related intermittent hypoxia trigger oxidative stress, systemic inflammation, and testicular dysfunction, leading to impaired sperm motility, abnormal morphology, and genomic instability. In OSA, the severity of reproductive disruption correlates with apnea-hypopnea index and nocturnal oxygen desaturation. Despite extensive evidence implicating metabolic and endocrine factors in male infertility, the role of sleep disturbances remains overlooked in clinical practice. Emerging evidence suggests that sleep disturbances may represent a relevant and potentially modifiable factor in male reproductive health. Interventions targeting sleep disorders and oxidative stress pathways have shown potential benefits on hormonal and physiological parameters; however, their direct impact on fertility outcomes remains to be established. Further longitudinal and interventional studies are needed to clarify causality and clinical applicability.

Loss of foxp3a drives sex-specific immune-metabolic remodeling across the gut-liver-gonad axis in zebrafish.

Modeling stimulus-induced stress responses in microglia-like cells using a commercial iPSC-dCas9-KRAB line.

In silico exploration of the RAPTOR-STAT3 interface reveals potential crosstalk between mTORC1 and JAK-STAT pathways in Sjogren's syndrome and its linked cancer.

Targeting TLR4 in Parkinson's disease: mechanisms and therapeutic prospects.

Huanglian Wendan ameliorates depression via gut-brain axis-related PPAR-α/allo pathways.

The neuroprotective role of eugenol against glyphosate-induced toxicity in rats: Modulation of oxidative stress, inflammation, ER stress and apoptotic signaling pathways.

Candida-bacteria interactions in peri-implantitis: A narrative review of evidence, mechanisms, and clinical implications.

Pre-eclampsia is a complex multisystem hypertensive disorder of pregnancy and a leading cause of maternal and perinatal morbidity and mortality worldwide. Increasing evidence suggests that the condition extends beyond abnormal placentation and represents an integrated immuno-cardiovascular disorder characterized by immune dysregulation, endothelial dysfunction, thromboinflammation, and cardiovascular maladaptation. This narrative review examines the interconnected mechanisms linking cytokine-mediated inflammation, endothelial injury, coagulation abnormalities, and maternal cardiovascular instability in pre-eclampsia. A structured literature search of major biomedical databases was conducted to identify relevant experimental, clinical, and translational studies addressing inflammatory cytokines, angiogenic imbalance, endothelial dysfunction, thrombosis, biomarkers, and therapeutic strategies in pre-eclampsia. The review highlights the central roles of pro-inflammatory mediators, including tumor necrosis factor-α, interleukin-6, interleukin-17, and interferon-γ, in promoting oxidative stress, vascular inflammation, and endothelial dysfunction. Particular attention is given to the development of an immunothrombotic environment, defined as the pathological interaction between immune activation and coagulation pathways that promotes thrombosis and vascular injury. The review also critically evaluates the contribution of antiangiogenic factors, platelet activation, impaired fibrinolysis, and cardiovascular remodeling to maternal disease progression. In addition, current and emerging therapeutic approaches targeting inflammatory, endothelial, angiogenic, and thrombotic pathways are discussed, together with their translational potential and clinical limitations. By integrating immunological, vascular, hematological, and cardiovascular perspectives, this review provides a comprehensive framework for understanding the pathophysiology of pre-eclampsia and identifies important knowledge gaps for future investigation.

P2X4 Drives Sex-Specific neuroprotection in autoimmune neuroinflammation.

Comparative toxicity of nickel titanate and calcium manganite perovskite nanomaterials in human and bacterial systems: Implications for environmental and health risks.

Melatonin ameliorates gastric mucosal damage induced by ethanol and heat stress: A comparative biochemical and histomorphometric study.

Dual-functional tea polyphenol-serotonin nanoparticles for integrated inflammation suppression and mucosal repair in inflammatory bowel disease.

Exploring the therapeutic potential of Radix Puerariae isoflavonoids against atherosclerosis through integrative network pharmacology and machine learning.

Peripheral to central: Exploring the neural, endocrine, and immune pathways of the gut-brain axis in postoperative neurocognitive dysfunction.

SIRT6 activation attenuates inflammatory-fibrogenic events, improves lung function and survival in experimental pulmonary fibrosis.