Results 121 to 130 of about 2,013 (228)

Glycative Stress Disrupts the Mitochondrial‐Lysosome Axis and Promotes Geroconversion in Aging Cardiomyocytes

open access: yesAging Cell, Volume 25, Issue 3, March 2026.
Cardiac aging promotes mitochondrial AGE accumulation driven by defective glycative stress detoxification. AGE‐modified mitochondria disrupt lysosomal proteolysis, impairing mitophagy and promoting lipofuscin buildup. This mechanism sustains chronic unresolved mitochondrial damage, driving proinflammatory senescence in cardiomyocytes and defining a ...
Diana Bou‐Teen   +13 more
wiley   +1 more source

PIK‐III‐Mediated Elevation of Thiamine Re‐Sensitises Renal Cell Carcinoma to Cuproptosis via Activating PDHA1

open access: yesCell Proliferation, Volume 59, Issue 3, March 2026.
PIK‐III enhancing the efficacy of cuproptosis to kill renal cancer cells through dysregulating thiamine metabolism and dephosphorylation of pyruvate dehydrogenase complex E1 (PDHA1), providing a potential option for treatment of cuproptosis‐resistant renal cancer by the combination of PIK‐III and elesclomol.
Dongdong Xie   +8 more
wiley   +1 more source

Astrocyte Bioenergetic Remodeling as a Central Trait of Disrupted Glucocorticoid Signaling: Mechanisms and Implications for Stress Vulnerability

open access: yesJournal of Neurochemistry, Volume 170, Issue 3, March 2026.
Low/brief glucocorticoid (GC) elevations can enhance mitochondrial output (↑ oxygen consumption rate, OCR; ↑ mitochondrial membrane potential, ΔΨm) and Ca2+ buffering, in part via glucocorticoid receptor (GR) trafficking to mitochondria in complexes with Bcl2 and Bag1.
Paweł Hanus   +2 more
wiley   +1 more source

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