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10.1038/s41467-025-67181-x http://scihub22266oqcxt.onion/10.1038/s41467-025-67181-x 41390760!?!41390760       Nat+Commun 2025 ; ? (?): ? Nephropedia Template TP {{tp|p=41390760|t=2025. Sodium disrupts mitochondrial energy metabolism to execute NECSO |pdf=|usr=}}{{41390760}} gab.com Text Sodium disrupts mitochondrial energy metabolism to execute NECSO JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=41390760 #FOAvip Na(+) influx is a critical pathological event in various conditions such as ischemia, hyperosmotic stress, and organ failure. Although persistent activation of the transient receptor potential cation channel subfamily M member 4 (TRPM4) by chemical agonist Necrocide 1 (NC1) triggers necrosis by sodium overload (NECSO), the underlying mechanism remains to be elucidated. Here, we demonstrate that Na(+) influx promotes necrosis by suppressing mitochondrial energy production. TRPM4-mediated Na(+) entry elevates mitochondrial Na(+) and reduces mitochondrial Ca(2)(+) via NCLX, inhibiting oxidative phosphorylation and the Trichloroacetic acid (TCA) cycle, leading to severe energy depletion. This results in Na/K-ATPase inactivation, loss of ion gradients, cellular swelling and lysis. Our study reveals how sodium overload in NECSO disrupts mitochondrial metabolism to cause energy failure, potentially underlying diseases with elevated Na(+). Twit Text FOAVip Sodium disrupts mitochondrial energy metabolism to execute NECSO ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=41390760 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41390760 #FOAvip English Wikipedia <ref>{{Cite pmid|41390760}}</ref> Sodium disrupts mitochondrial energy metabolism to execute NECSO #MMPMID41390760 Qiao Y; Wang J; Wang B; Zhou H; Ni Q; Fu W; Hu Z; Zhong Q Nat Commun 2025[Dec]; ? (?): ? PMID41390760show ga Na(+) influx is a critical pathological event in various conditions such as ischemia, hyperosmotic stress, and organ failure. Although persistent activation of the transient receptor potential cation channel subfamily M member 4 (TRPM4) by chemical agonist Necrocide 1 (NC1) triggers necrosis by sodium overload (NECSO), the underlying mechanism remains to be elucidated. Here, we demonstrate that Na(+) influx promotes necrosis by suppressing mitochondrial energy production. TRPM4-mediated Na(+) entry elevates mitochondrial Na(+) and reduces mitochondrial Ca(2)(+) via NCLX, inhibiting oxidative phosphorylation and the Trichloroacetic acid (TCA) cycle, leading to severe energy depletion. This results in Na/K-ATPase inactivation, loss of ion gradients, cellular swelling and lysis. Our study reveals how sodium overload in NECSO disrupts mitochondrial metabolism to cause energy failure, potentially underlying diseases with elevated Na(+). ?Sodium disrupts mitochondrial energy metabolism to execute NECSO (epmc).pdf DeepDyve Pubget Overpricing