Building on previous work (Fu et al., 2016), we demonstrate the critical role of Sam68 in orchestrating genotoxic stress-initiated NF-κB signaling in the colon and the pathophysiological relevance of Sam68-dependent NF-κB activation in colonic cell survival/recovery from extrinsic DNA damage.
Brain natriuretic peptide supplementation can increase cardiac neovascularization in infarcted hearts by stimulating endogenous endothelial cell proliferation and proliferation of precursor cells, which will differentiate into endothelial cells.
Multi-omics reveals that Alkb homolog 7 (ALKBH7), α mitochondrial alpha-ketoglutarate dioxygenase of unclear function, regulates glyoxal metabolism, which may explain its role in necrosis and heart attack.
Cardiomyocyte Nox4 is a crucial physiological mediator of Nrf2 activation during acute exercise, triggering an adaptive response that preserves redox balance, mitochondrial and cardiac function to support normal physical exercise.
β3-AR signalling via cGMP in cardiomyocytes is regulated via phosphodiesterase 2 and 5 degradation, it is potentially cardioprotective, but dysregulated in heart failure through signal redistribution and higher phosphodiesterase activity.
Mitophagy regulates mitochondrial quality and mediates extensive mitochondrial degradation in (patho-)physiological settings and is one of the key components of hypoxic preconditioning which protects the heart from ischemia/reperfusion injury.
EPO/JAK2/PKA signaling cascade via AKAP10 relocalization to the outer mitochondrial membrane results in the phosphorylation of the terminal heme synthesis enzyme ferrochelatase, which contributes to heme production in red cells.