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10.1007/s00018-025-05960-x http://scihub22266oqcxt.onion/10.1007/s00018-025-05960-x 41359167!?!41359167 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=41359167&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       Cell+Mol+Life+Sci 2025 ; 82 (1): 437 Nephropedia Template TP {{tp|p=41359167|t=2025. Stress-Induced calcium mishandling in cardiac (Patho)physiology |pdf=|usr=}}{{41359167}} gab.com Text Stress-Induced calcium mishandling in cardiac (Patho)physiology JO: Cell Mol Life Sci http://www.kidney.de/pget.php?&tw=1&pmid=41359167 #FOAvip Calcium (Ca(2+)) is an essential regulator of cardiac function. Particularly, Ca(2+) is the primary link between the electrical signals regulating contractility of the myocytes and thus allowing the heart chambers to relax and refill completely with blood. Additionally, Ca(2+) controls numerous other activities including gene transcription, cell growth, and survival. The abnormal Ca(2+) regulation and cycling in the cardiomyocyte following various stressor's, insults and during cardiac disease development has been found to be a primary culprit leading to cellular dysfunction and potentially to cell death and ultimately resulting in impaired cardiac function and disease development. This review aims to briefly describe our current understanding regarding the role of Ca(2+) signaling in cardiac function under physiological and stressed conditions. Twit Text FOAVip Stress-Induced calcium mishandling in cardiac (Patho)physiology ????Cell Mol Life Sci http://www.kidney.de/pget.php?&tw=1&pmid=41359167 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41359167 #FOAvip English Wikipedia <ref>{{Cite pmid|41359167}}</ref> Stress-Induced calcium mishandling in cardiac (Patho)physiology #MMPMID41359167 Bare DJ; Ai X Cell Mol Life Sci 2025[Dec]; 82 (1): 437 PMID41359167show ga Calcium (Ca(2+)) is an essential regulator of cardiac function. Particularly, Ca(2+) is the primary link between the electrical signals regulating contractility of the myocytes and thus allowing the heart chambers to relax and refill completely with blood. Additionally, Ca(2+) controls numerous other activities including gene transcription, cell growth, and survival. The abnormal Ca(2+) regulation and cycling in the cardiomyocyte following various stressor's, insults and during cardiac disease development has been found to be a primary culprit leading to cellular dysfunction and potentially to cell death and ultimately resulting in impaired cardiac function and disease development. This review aims to briefly describe our current understanding regarding the role of Ca(2+) signaling in cardiac function under physiological and stressed conditions. |*Calcium Signaling[MESH] |*Calcium/metabolism[MESH] |*Heart/physiology/physiopathology[MESH] |*Myocardium/metabolism/pathology[MESH] |*Myocytes, Cardiac/metabolism[MESH] |*Stress, Physiological[MESH] |Animals[MESH] |Heart Diseases/metabolism/pathology[MESH]Stress-Induced calcium mishandling in cardiac (Patho)physiology (epmc).pdf DeepDyve Pubget Overpricing