Human infertility represents a multifaceted condition, with oxidative stress (OS) and microRNAs (miRNAs) emerging as key contributors to its pathophysiology. This comprehensive review explores the complex interplay between reactive oxygen …
With each menstrual cycle, endometrial cells rapidly proliferate and decidualize in preparation for pregnancy. Such rapid proliferation generates replication stress and results in DNA damage with irreparable cells undergoing senescence. …
Endometriosis is a chronic inflammatory disease characterized by pelvic pain and infertility, with oxidative stress playing a key role in its pathogenesis. Although antioxidant supplementation has been proposed as a …
Ultrastructural evaluation of lithium-induced autophagic and mitochondrial stress in 3D endometrial and neuroblastoma spheroids Nature
Zishen Quyu Jiedu formula (ZQYJDF) is a commonly used prescription for endometriosis (EMs) with clinical efficacy. However, its active components and potential mechanisms remain unknown. This study aimed to identify …
Endometriosis is a prevalent chronic inflammatory condition impacting 5-10% of reproductive-age women, commonly resulting in debilitating pelvic pain and infertility. Despite extensive research efforts, the precise underlying pathophysiology remains largely …
Background/Objectives: Endometriosis (EM) is a chronic gynecological condition associated with infertility, oxidative stress, and altered metabolic regulation. Follicular fluid (FF) reflects the microenvironment of the developing oocyte, and changes in …
Endometriosis (EMS) is a chronic gynecological disease. RND3 is recognized as a potential autophagy-related biomarker in EMS. The aim of this study was to investigate the regulatory role of RND3 …
Ferroptosis is a novel kind of regulated cell death that occurs when redox equilibrium is disrupted, leading to iron-dependent lipid peroxidation. Ferroptosis is defined by the buildup of deleterious lipid …
Disulfidptosis is a novel Nicotinamide Adenine Dinucleotide Phosphate (NADPH) deficiency-driven cell death pathway characterized by cystine overload and aberrant disulfide bond formation in actin cytoskeletal proteins, distinct from apoptosis, ferroptosis, …