Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.3389/fphys.2019.01277 http://scihub22266oqcxt.onion/10.3389/fphys.2019.01277 31636573!6787934!31636573     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=31636573&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Front+Physiol 2019 ; 10 (?): 1277 Nephropedia Template TP {{tp|p=31636573|t=2019. Enhancing Autophagy Diminishes Aberrant Ca(2+) Homeostasis and Arrhythmogenesis in Aging Rabbit Hearts |pdf=|usr=}}{{31636573}} gab.com Text Enhancing Autophagy Diminishes Aberrant Ca(2+) Homeostasis and Arrhythmogenesis in Aging Rabbit Hearts JO: Front Physiol http://www.kidney.de/pget.php?&tw=1&pmid=31636573 #FOAvip AIM: Aging in humans is associated with a 10-40-fold greater incidence of sudden cardiac death from malignant tachyarrhythmia. We have reported that thiol oxidation of ryanodine receptors (RyR2s) by mitochondria-derived reactive oxygen species (mito-ROS) contributes to defective Ca(2+) homeostasis in cardiomyocytes (CMs) from aging rabbit hearts. However, mechanisms responsible for the increase in mito-ROS in the aging heart remain poorly understood. Here we test the hypothesis that age-associated decrease in autophagy is a major contributor to enhanced mito-ROS production and thereby pro-arrhythmic disturbances in Ca(2+) homeostasis. METHODS AND RESULTS: Ventricular tissues from aged rabbits displayed significant downregulation of proteins involved in mitochondrial autophagy compared with tissues from young controls. Blocking autophagy with chloroquine increased total ROS production in primary rabbit CMs and mito-ROS production in HL-1 CMs. Furthermore, chloroquine treatment of HL-1 cells depolarized mitochondrial membrane potential (Deltapsim) to 50% that of controls. Blocking autophagy significantly increased oxidation of RyR2, resulting in enhanced propensity to pro-arrhythmic spontaneous Ca(2+) release under beta-adrenergic stimulation. Aberrant Ca(2+) release was abolished by treatment with the mito-ROS scavenger mito-TEMPO. Importantly, the autophagy enhancer Torin1 and ATG7 overexpression reduced the rate of mito-ROS production and restored both Deltapsim and defective Ca(2+) handling in CMs derived from aged rabbit hearts. CONCLUSION: Decreased autophagy is a major cause of increased mito-ROS production in the aging heart. Our data suggest that promoting autophagy may reduce pathologic mito-ROS during normal aging and reduce pro-arrhythmic spontaneous Ca(2+) release via oxidized RyR2s. Twit Text FOAVip Enhancing Autophagy Diminishes Aberrant Ca(2+) Homeostasis and Arrhythmogenesis in Aging Rabbit Hearts ????Front Physiol http://www.kidney.de/pget.php?&tw=1&pmid=31636573 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31636573 #FOAvip English Wikipedia <ref>{{Cite pmid|31636573}}</ref> Enhancing Autophagy Diminishes Aberrant Ca(2+) Homeostasis and Arrhythmogenesis in Aging Rabbit Hearts #MMPMID31636573 Murphy KR; Baggett B; Cooper LL; Lu Y; O-Uchi J; Sedivy JM; Terentyev D; Koren G Front Physiol 2019[]; 10 (?): 1277 PMID31636573show ga AIM: Aging in humans is associated with a 10-40-fold greater incidence of sudden cardiac death from malignant tachyarrhythmia. We have reported that thiol oxidation of ryanodine receptors (RyR2s) by mitochondria-derived reactive oxygen species (mito-ROS) contributes to defective Ca(2+) homeostasis in cardiomyocytes (CMs) from aging rabbit hearts. However, mechanisms responsible for the increase in mito-ROS in the aging heart remain poorly understood. Here we test the hypothesis that age-associated decrease in autophagy is a major contributor to enhanced mito-ROS production and thereby pro-arrhythmic disturbances in Ca(2+) homeostasis. METHODS AND RESULTS: Ventricular tissues from aged rabbits displayed significant downregulation of proteins involved in mitochondrial autophagy compared with tissues from young controls. Blocking autophagy with chloroquine increased total ROS production in primary rabbit CMs and mito-ROS production in HL-1 CMs. Furthermore, chloroquine treatment of HL-1 cells depolarized mitochondrial membrane potential (Deltapsim) to 50% that of controls. Blocking autophagy significantly increased oxidation of RyR2, resulting in enhanced propensity to pro-arrhythmic spontaneous Ca(2+) release under beta-adrenergic stimulation. Aberrant Ca(2+) release was abolished by treatment with the mito-ROS scavenger mito-TEMPO. Importantly, the autophagy enhancer Torin1 and ATG7 overexpression reduced the rate of mito-ROS production and restored both Deltapsim and defective Ca(2+) handling in CMs derived from aged rabbit hearts. CONCLUSION: Decreased autophagy is a major cause of increased mito-ROS production in the aging heart. Our data suggest that promoting autophagy may reduce pathologic mito-ROS during normal aging and reduce pro-arrhythmic spontaneous Ca(2+) release via oxidized RyR2s. ?Enhancing Autophagy Diminishes Aberrant Ca(2+) Homeostasis and Arrhyth(epmc).pdf DeepDyve Pubget Overpricing