Heart remodeling occurs as a compensation mechanism for the massive loss of tissue during initial heart failure and the consequent inflammation process. During heart remodeling fibroblasts differentiate to myofibroblasts activate their secretion functions and produce elevated amounts, of extracellular matrix (ECM) proteins, mostly collagen, that form scar tissue and alter the normal degradation of ECM. Scar formation does replace the damaged tissue structurally; however, it impedes the normal contractive function of cardiomyocytes (CMs) and results in longlasting effects after heart failure. Besides CMs and cardiac fibroblasts, endothelial cells (ECs) and circulating endothelial progenitor cells (cEPCs) contribute to heart repair. This review summarizes the current knowledge of EC-CM crosstalk in cardiac fibrosis (CF), the role of cEPCs in heart regeneration and the contribution of Endothelial-mesenchymal transition (EndoMT)., Barbara Šalingová, Zdenko Červenák, Andriana Adamičková, Nikola Chromanicová, Simona Valášková, Andrea Gažová, Ján Kyselovič., and Obsahuje bibliografii
We studied the role of the δ, µ, and к opioid receptor (OR)
subtypes in the cardioprotective effect of chronic continuous
normobaric hypoxia (CNH) in the model of acuteanoxia/
reoxygenation of isolated cardiomyocytes. Adaptation of rats to
CNH was performed by their exposure to atmosphere containing
12 % of O2 for 21 days. Anoxia/reoxygenation of cardiomyocytes
isolated from normoxic control rats caused the death of 51 % of
cells and lactate dehydrogenase (LDH) release. Adaptation of rats
to CNH resulted in the anoxia/reoxygenation-induced
cardiomyocyte death of only 38 %, and reduced the LDH release.
Pre-incubation of the cells with either the non-selective OR
blocker naloxone (300 nM/l), the δ OR antagonist TIPP(ψ)
(30 nM/l), the selective δ2 OR antagonist naltriben (1 nM/l) or the
μ OR antagonist CTAP (100 nM/l) for 25 minutes before anoxia
abolished the reduction of cell death and LDH release afforded by
CNH. The antagonist of δ1 OR BNTX (1 nM/l) or the κ OR
antagonist nor-binaltorphimine (3 nM/l) did not influence the
cytoprotective effects of CNH. Taken together, the cytoprotective
effect of CNH is associated with the activation of the δ2 and μ OR
localized on cardiomyocytes.
Autophagy is implicated in the maintenance of cardiac homeostasis. Autophagy is activated in heart failure, in which reactive oxygen species (ROS) are increased. Exogenous ROS have been shown to induce cardiomyocyte autophagy alterations. However, little is known about the influences of physiological levels of endogenous ROS on cardiomyocyte autophagy. In the present study, we tested the hypothesis that endogenous ROS in cardiomyocytes play an important role in inducing autophagy. Cultured H9C2 cardiomyocytes or Sprague-Dawley rats were treated with the antioxidant N-acetyl-cysteine (NAC) or the superoxide dismutase mimic tempol under the basal or nutrient deprivation conditions. The autophagic flux was assessed by the lysosomal inhibitor chloroquine. In H9C2 cardiomyocytes, under a basal condition, NAC or tempol increased the ratio of LC3 II/I proteins and reduced LC3 II autophagic flux. Under nutrient deprivation, NAC increased the LC3 II/I ratio and reduced LC3 II autophagic flux. In vivo studies in rats, NAC treatment increased the LC3 II/I ratio and p-Akt protein expression in myocardium. We concluded that the antioxidants reduced autophagic flux in cardiomyocytes under the basal or nutrient deprivation conditions, suggesting that endogenous ROS promote autophagy flux under physiological conditions, and this effect is mediated, at least in part, through Akt inhibition., J.-P. Wang, R.-F. Chi, J. Liu, Y.-Z. Deng, X.-B. Han, F.-Z. Qin, B. Li., and Seznam literatury