Endometriosis is an estrogen-dependent benign disease characterized by the development of endometrial tissue outside the uterus. This intricate ailment markedly affects a patient's well-being and lacks a definitive cure. Endometriotic cells enhance their viability by modulating genetic and epigenetic characteristics, with mitochondria being important organelles in determining cellular metabolic pathways. Mitochondrial malfunction is associated with various human disorders, and the disruption of mitochondrial adaptation mechanisms may help develop new therapies for endometriosis. This article examines the significance of mitochondrial balance in the etiology and advancement of endometriosis and introduces several potential drugs targeting mitochondria for its treatment.
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http://dx.doi.org/10.1007/s43032-025-01827-5 | DOI Listing |
J Cell Sci
March 2025
Department of Biochemistry, University of Utah School of Medicine, Salt Lake City, UT 84112, USA.
Mitochondria perform diverse functions, such as producing ATP through oxidative phosphorylation, synthesizing macromolecule precursors, maintaining redox balance, and many others. Given this diversity of functions, we and others have hypothesized that cells maintain specialized subpopulations of mitochondria. To begin addressing this hypothesis, we developed a new dual-purification system to isolate subpopulations of mitochondria for chemical and biochemical analyses.
View Article and Find Full Text PDFStem Cells Dev
March 2025
Center for Genomic Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.
Orchestrated changes in cell arrangements and cell-to-cell contacts are susceptible to cellular stressors during central nervous system development. Effects of mitochondrial complex I inhibition on cell-to-cell contacts have been studied in vascular and intestinal structures; however, its effects on developing neuronal cells are largely unknown. We investigated the effects of the classical mitochondrial stressor and complex I inhibitor, rotenone, on the architecture of neural rosettes-radially organized neuronal progenitor cells (NPCs)-differentiated from human-induced pluripotent stem cells.
View Article and Find Full Text PDFHaematologica
March 2025
Division of Haematology and Haemostaseology, Department of Medicine I, Medical University of Vienna; Vienna.
Hemophilia is a rare X-linked bleeding disorder caused by mutations in the F8 or F9 gene (hemophilia A or B), leading to deficient factor VIII or IX proteins, respectively. Hemophilia-related complications caused by bleeding into the joints (the hallmark of hemophilia) and age-related comorbidities occur frequently and impact the functionality and quality of life of persons with hemophilia (PwH). Given the chronic nature of hemophilia, we hypothesized that hemophilia has an association with accelerated biological aging.
View Article and Find Full Text PDFAdv Healthc Mater
March 2025
Department of Orthopaedics, Key Laboratory of Structural Malformations in Children of Zhejiang Province, Key Laboratory of Orthopaedics of Zhejiang Province, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Intervertebral disc degeneration (IVDD) is a major cause of low back pain, where oxidative stress and mitochondrial dysfunction are key contributors. Additionally, ferroptosis, an iron-dependent form of cell death, is identified as a critical mechanism in IVDD pathogenesis. Herein, the therapeutic potential of gallic acid (GA)-derived PGA-Cu nanoparticles, enhanced with functional octapeptide (Cys-Lys-His-Gly-d-Arg-d-Tyr-Lys-Phe, SS08) to build the mitochondria-targeted nanoparticles (PGA-Cu@SS08), and embedded within a hydrogel matrix to form a nanocomposite hydrogel, is explored.
View Article and Find Full Text PDFWellcome Open Res
February 2025
Syngenta International Research Station, Jealott's Hill, Berkshire, England, UK.
We present a genome assembly from a male specimen of (flea beetle; Arthropoda; Insecta; Coleoptera; Chrysomelidae). The genome sequence has a total length of 671.30 megabases.
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