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10.1002/cmdc.202500968 http://scihub22266oqcxt.onion/10.1002/cmdc.202500968 41319342!?!41319342 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=41319342&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       ChemMedChem 2025 ; ? (?): e202500968 Nephropedia Template TP {{tp|p=41319342|t=2025. Small-Molecule Sarco/Endoplasmic Reticulum Ca(2+)-ATPase Activators Reverse Methylglyoxal-Induced Inhibition through Nonantioxidant Mechanisms |pdf=|usr=}}{{41319342}} gab.com Text Small-Molecule Sarco/Endoplasmic Reticulum Ca(2+)-ATPase Activators Reverse Methylglyoxal-Induced Inhibition through Nonantioxidant Mechanisms JO: ChemMedChem http://www.kidney.de/pget.php?&tw=1&pmid=41319342 #FOAvip Impaired endoplasmic reticulum (ER) Ca(2+) homeostasis contributes to beta-cell dysfunction under diabetic stressors such as methylglyoxal (MGX), a reactive byproduct that induces oxidative protein modifications and advanced glycation end-products. The calcium pump sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA), essential for ER Ca(2+) regulation, is inhibited by MGX-mediated carbonylation and thiol oxidation. Pharmacological SERCA activation has emerged as a promising strategy to restore ER Ca(2+) balance, but whether protection results from direct allosteric modulation, indirect antioxidant effects, or both has remained unclear. Herein, it is shown that novel, potent synthetic activators directly stimulate SERCA and restore its activity following MGX-induced inhibition. While some compounds display antioxidant activity, recovery of SERCA function correlated with activation potency rather than radical scavenging or lipid peroxidation inhibition. It is demonstrated for the first time that direct SERCA activation alone is sufficient to significantly reverse oxidative damage, revealing a mechanistically distinct therapeutic approach to preserve ER Ca(2+) homeostasis in diabetes. Twit Text FOAVip Small-Molecule Sarco/Endoplasmic Reticulum Ca(2+)-ATPase Activators Reverse Methylglyoxal-Induced Inhibition through Nonantioxidant Mechanisms ????ChemMedChem http://www.kidney.de/pget.php?&tw=1&pmid=41319342 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41319342 #FOAvip English Wikipedia <ref>{{Cite pmid|41319342}}</ref> Small-Molecule Sarco/Endoplasmic Reticulum Ca(2+)-ATPase Activators Reverse Methylglyoxal-Induced Inhibition through Nonantioxidant Mechanisms #MMPMID41319342 Cruz-Cortes C; Michalikova S; Rezbarikova P; Espinoza-Fonseca LM; Viskupicova J ChemMedChem 2025[Nov]; ? (?): e202500968 PMID41319342show ga Impaired endoplasmic reticulum (ER) Ca(2+) homeostasis contributes to beta-cell dysfunction under diabetic stressors such as methylglyoxal (MGX), a reactive byproduct that induces oxidative protein modifications and advanced glycation end-products. The calcium pump sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA), essential for ER Ca(2+) regulation, is inhibited by MGX-mediated carbonylation and thiol oxidation. Pharmacological SERCA activation has emerged as a promising strategy to restore ER Ca(2+) balance, but whether protection results from direct allosteric modulation, indirect antioxidant effects, or both has remained unclear. Herein, it is shown that novel, potent synthetic activators directly stimulate SERCA and restore its activity following MGX-induced inhibition. While some compounds display antioxidant activity, recovery of SERCA function correlated with activation potency rather than radical scavenging or lipid peroxidation inhibition. It is demonstrated for the first time that direct SERCA activation alone is sufficient to significantly reverse oxidative damage, revealing a mechanistically distinct therapeutic approach to preserve ER Ca(2+) homeostasis in diabetes. ?Small-Molecule Sarco/Endoplasmic Reticulum Ca(2+)-ATPase Activators Re(epmc).pdf DeepDyve Pubget Overpricing