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Artery calcification is a well-recognized predictor of late atherosclerotic complications. In the intima media, calcification starts with apoptosis of vascular smooth muscle cells (VSMCs) and the release of calcifying matrix vesicles with diameter of 0.5-15 m that can be observed microscopically. In complicated plaques, calcification is generally less frequent. Calcifying vesicles are released by proatherosclerotic VSMCs into the collagen-rich matrix. The vesicles can penetrate into the intima media and protrude into the arterial lumen and thereby may represent a potential cause of atherothrombosis. In calcified fibrolipid plaques, the rate of calcification is increased but is followed with healing of a lesion rupture and exhibited by further erosion and/or intimal thickening. Generally, calcification directly correlates with the apoptosis of VSMCs and macrophages accompanied by the release of osteogenic matrix vesicles. This is a hallmark of atherosclerosis-related apoptosis of VSMCs that is commonly released in plaque stabilization.
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http://dx.doi.org/10.1155/2017/7463590 | DOI Listing |
Dev Growth Differ
September 2025
Department of Biological Sciences, College of Arts, Sciences, and Education, Florida International University, Miami, Florida, USA.
Superoxide dismutases (SODs) are key regulators of reactive oxygen species (ROS) and redox balance. Although intracellular SODs have been extensively studied, growing attention has been directed toward understanding the roles of extracellular SODs in both Dictyostelium and mammalian systems. In Dictyostelium discoideum, SodC is a glycosylphosphatidylinositol (GPI)-anchored enzyme that modulates extracellular superoxide to regulate Ras, PI3K signaling, and cytoskeletal remodeling during directional cell migration.
View Article and Find Full Text PDFCancer Metastasis Rev
September 2025
Institute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS, Gif-Sur-Yvette, 91198, France.
Integrins constitute a large and diverse family of cell adhesion molecules that play essential roles in regulating tumor cell differentiation, migration, proliferation, and neovascularization. Tumor cell-derived exosomes, a subtype of extracellular vesicles, are enriched with integrins that reflect their cells of origin. These exosomal integrins can promote extracellular matrix remodeling, immune suppression, and vascular remodeling and are closely linked to tumor progression and metastasis, acting as pivotal players in mediating organ-specific metastasis.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
August 2025
Division of Biochemistry and Molecular Biology, Siberian State Medical University, Ministry of Health of the Russian Federation, 634050 Tomsk, Russia.
Background: Sarcopenia is a complex, multifactorial condition characterized by progressive loss of muscle mass, strength, and function. Despite growing awareness, the early diagnosis and pathophysiological characterization of this condition remain challenging due to the lack of integrative biomarkers.
Objective: This study aimed to conduct a comprehensive multilevel profiling of clinical parameters, immune cell phenotypes, extracellular vesicle (EV) signatures, and biochemical markers to elucidate biological gradients associated with different stages of sarcopenia.
Chem Biol Interact
September 2025
Department of Human Development and Family Studies, National Taiwan Normal University, Taipei, 10610, Taiwan; Graduate Program of Nutrition Science, School of Life Science, National Taiwan Normal University, Taipei, 11677, Taiwan. Electronic address:
Accumulated dysfunctional mitochondria are involved in tumorigenesis, and it is conceivable that mitophagy, a selective form of autophagic degradation of mitochondria, plays a tumor-suppressive role. Our bioinformatics analysis identified lignan justicidin A (JA) as a potential mitophagy inducer. In HRAS-mutant human bladder cancer T24 cells, JA reduced population cell growth, changed mitochondrial membrane potential, and induced autophagy.
View Article and Find Full Text PDFBiology (Basel)
August 2025
Department of Oral Biology, The Dental College of Georgia, Augusta University, Augusta, GA 30912, USA.
The retina is highly sensitive to oxygen and blood supply, and hypoxia plays a key role in retinal diseases such as diabetic retinopathy (DR) and age-related macular degeneration (AMD). Müller glial cells, which are essential for retinal homeostasis, respond to injury and hypoxia with reactive gliosis, characterized by the upregulation of the glial fibrillary acidic protein (GFAP) and vimentin, cellular hypertrophy, and extracellular matrix changes, which can impair retinal function and repair. The retinal pigment epithelium (RPE) supports photoreceptors, forms part of the blood-retinal barrier, and protects against oxidative stress; its dysfunction contributes to retinal degenerative diseases such as AMD, retinitis pigmentosa (RP), and Stargardt disease (SD).
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