SERCA2 phosphorylation at serine 663 is a key regulator of Ca²⁺ homeostasis in heart diseases.

ABSTRACT: Despite advances in cardioprotection, new therapeutic strategies capable of preventing ischemia-reperfusion injury of patients are still needed. Here, we discover that sarcoplasmic/endoplasmic reticulum Ca²⁺ ATPase (SERCA2) phosphorylation at serine 663 is a clinical and pathophysiological event of cardiac function. Indeed, the phosphorylation level of SERCA2 at serine 663 is increased in ischemic hearts of patients and mouse. Analyses on different human cell lines indicate that preventing serine 663 phosphorylation significantly increases SERCA2 activity and protects against cell death, by counteracting cytosolic and mitochondrial Ca²⁺ overload. By identifying the phosphorylation level of SERCA2 at serine 663 as an essential regulator of SERCA2 activity, Ca²⁺

SUBMITTER: Gonnot F 

PROVIDER: S-EPMC10250397 | biostudies-literature | 2023 Jun

REPOSITORIES: biostudies-literature