Publications by authors named "Kulczyk J"
Article Synopsis
- The study explores metabolic changes in aged myoblasts, revealing that they face issues like poor glycolysis and insulin resistance, particularly in both human and mouse models of aging.
- It was found that senescent myoblasts produce excess ammonium through a specific metabolic pathway involving methionine, which can contribute to aging effects.
- By manipulating factors like the NANOG protein or inhibiting a specific enzyme (methionine adenosyltransferase 2A), researchers enhanced muscle regeneration and strength, suggesting that altering methionine metabolism could counteract age-related muscle decline.
Senescence of myogenic progenitors impedes skeletal muscle regeneration. Here, we show that overexpression of the transcription factor NANOG in senescent myoblasts can overcome the effects of cellular senescence and confer a youthful phenotype to senescent cells. NANOG ameliorated primary hallmarks of cellular senescence including genomic instability, loss of proteostasis, and mitochondrial dysfunction.
View Article and Find Full Text PDFThe aims of this work were to determine: 1) whether Ca2+ exit via the plasmalemmal Ca2+ ATPase (PMCA) is coupled to H+ entry via a Ca2+/H+ exchange; 2) whether operation of PMCA has an absolute requirement on external H+ (Ho); and 3) the stoichiometry and voltage-dependence of the Ca2+/H+ exchange. Barnacle muscle cells were used because of the ease with which they can be internally-perfused (e.g.
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