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10.1007/s10557-025-07809-8 http://scihub22266oqcxt.onion/10.1007/s10557-025-07809-8 41389127!?!41389127 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=41389127&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       Cardiovasc+Drugs+Ther 2025 ; ? (?): ? Nephropedia Template TP {{tp|p=41389127|t=2025. Crosstalk between Ryanodine Receptor 2 Dysfunction and FK506-Binding Proteins in Pulmonary Hypertension |pdf=|usr=}}{{41389127}} gab.com Text Crosstalk between Ryanodine Receptor 2 Dysfunction and FK506-Binding Proteins in Pulmonary Hypertension JO: Cardiovasc Drugs Ther http://www.kidney.de/pget.php?&tw=1&pmid=41389127 #FOAvip BACKGROUND: Pulmonary hypertension (PH) is a complicated cardiovascular disorder marked by elevated pulmonary arterial pressure and vascular remodeling. The molecular interplay between Ryanodine Receptor 2 (RyR2) and FK506-binding protein 12.6 (FKBP12.6) emphasizes that their dissociation under hypoxic conditions results in intracellular calcium(Ca(2)(+)) dysregulation in pulmonary artery smooth muscle cells (PASMCs). OBJECTIVE: This review article highlights important discoveries about how mitochondrial ROS, particularly those mediated by the Rieske iron-sulfur protein (RISP), trigger RyR2 activation and the sub sequent release of Ca2+. Furthermore, it covers a process that establishes a connection between sarcoplasmic reticulum calcium signaling, which promotes vasoconstriction and vascular remodeling, and mitochondrial dysfunction. CONCLUSION: The pathways involved inRyR2/FKBP12.6 destabilization lead to progression in PH. Moreover, targeting these pathways has been reported to be beneficial in PH management. Twit Text FOAVip Crosstalk between Ryanodine Receptor 2 Dysfunction and FK506-Binding Proteins in Pulmonary Hypertension ????Cardiovasc Drugs Ther http://www.kidney.de/pget.php?&tw=1&pmid=41389127 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41389127 #FOAvip English Wikipedia <ref>{{Cite pmid|41389127}}</ref> Crosstalk between Ryanodine Receptor 2 Dysfunction and FK506-Binding Proteins in Pulmonary Hypertension #MMPMID41389127 Patel J; Doshi G Cardiovasc Drugs Ther 2025[Dec]; ? (?): ? PMID41389127show ga BACKGROUND: Pulmonary hypertension (PH) is a complicated cardiovascular disorder marked by elevated pulmonary arterial pressure and vascular remodeling. The molecular interplay between Ryanodine Receptor 2 (RyR2) and FK506-binding protein 12.6 (FKBP12.6) emphasizes that their dissociation under hypoxic conditions results in intracellular calcium(Ca(2)(+)) dysregulation in pulmonary artery smooth muscle cells (PASMCs). OBJECTIVE: This review article highlights important discoveries about how mitochondrial ROS, particularly those mediated by the Rieske iron-sulfur protein (RISP), trigger RyR2 activation and the sub sequent release of Ca2+. Furthermore, it covers a process that establishes a connection between sarcoplasmic reticulum calcium signaling, which promotes vasoconstriction and vascular remodeling, and mitochondrial dysfunction. CONCLUSION: The pathways involved inRyR2/FKBP12.6 destabilization lead to progression in PH. Moreover, targeting these pathways has been reported to be beneficial in PH management. ?Crosstalk between Ryanodine Receptor 2 Dysfunction and FK506-Binding P(epmc).pdf DeepDyve Pubget Overpricing