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Piezo1 mediates hypoxia-induced endometriosis fibrosis via the mtDNA -dependent cGAS-STING pathway.

Endometriosis (EMs) is a prevalent gynecological disorder characterized by the ectopic growth of functional endometrial tissue, and its fibrotic pathology represents a primary contributor to chronic pain and infertility in …

Published: May 19, 2026, midnight
Multi-omics Mendelian randomization identifies mitochondrial genes associated with immune microenvironment signatures in endometriosis.

Endometriosis is a complex gynaecological disorder that affects 10%-15% of reproductive-age women and is characterized by chronic inflammation, pelvic pain, and infertility. Although mitochondrial dysfunction is implicated in endometriosis pathogenesis, …

Published: May 4, 2026, midnight
Advancing the frontiers of phytotherapy: a comprehensive review of botanical interventions targeting mitochondrial quality control to ameliorate endometriosis.

Endometriosis (EMs) is a gynecological disorder affecting women of reproductive age. It is characterized by the ectopic implantation and infiltration of endometrial-like tissue and is associated with significant effects on …

Published: April 29, 2026, midnight
NET-DNA Activates the ANXA2/TMEM215/BiP Axis to Promote Mitophagy-Mediated Anoikis Resistance in Endometriosis.

Endometriosis (EMs) features ectopic implantation of endometrial stromal cells (EESCs) and strong anoikis resistance, yet how inflammatory signals reprogram mitochondrial function remains unclear. Here, neutrophil extracellular traps (NETs), particularly their …

Published: April 27, 2026, midnight
Extracellular Matrix Remodeling and Matrix Metalloproteinases in Ovarian Function and Infertility.

Ovarian function relies on a network of well-coordinated molecular mechanisms that regulate follicular development, oocyte maturation, ovulation, and corpus luteum function. When these processes are disrupted, infertility can result. Extracellular …

Published: April 19, 2026, midnight
Pelargonium graveolens Essential Oil Suppresses Proliferation and Migration and Modulates Mesenchymal-Associated Cellular Functions in Human Endometriotic Cells.

Endometriosis is characterized by enhanced cellular proliferation, migration, and resistance to apoptosis, contributing to lesion persistence and progression. Targeting cellular plasticity and mesenchymal-associated functions may therefore represent a promising therapeutic …

Published: April 15, 2026, midnight
CHCHD2: a bi-organellar fulcrum of mitochondrial homeostasis and reproductive pathology.

Mitochondrial dysfunction has been demonstrated with a role in pathologically driving various obstetric and gynecological (OB/GYN) diseases, but molecular mediators associating mitochondrial dysfunction with discrete pathologies have not been determined …

Published: April 13, 2026, midnight
Oocyte aging in focus: Environmental and endogenous stressors driving reproductive potential decline.

Oocyte quality, a critical determinant of female reproductive potential, experiences a progressive decline with age, largely driven by the cumulative effects of oxidative stress and mitochondrial dysfunction. This review thoroughly …

Published: April 9, 2026, midnight
Mechanisms of reproductive toxicity and endocrine disruption of bisphenols and per- and polyfluoroalkyl substances (PFAS): Implications for women's reproductive health.

Bisphenols and per- and polyfluoroalkyl substances (PFAS) are ubiquitous environmental endocrine-disrupting chemicals with widespread human exposure and growing concern regarding their reproductive toxicity. This review integrates current experimental and epidemiologic …

Published: April 9, 2026, midnight
Prenatal bisphenol A exposure reprograms SF1-lactylation pathways to promote endometriosis susceptibility.

Endometriosis is an estrogen-dependent disorder influenced by dysregulated steroidogenesis, oxidative stress, and inflammation. Bisphenol A (BPA), a common endocrine disruptor, has been associated with reproductive dysfunction, but its developmental impacts …

Published: April 4, 2026, midnight
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