2021
DOI: 10.1155/2021/6617816
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RIPK3‐Mediated Necroptosis in Diabetic Cardiomyopathy Requires CaMKII Activation

Abstract: Activation of Ca2+/calmodulin-dependent protein kinase (CaMKII) has been proved to play a vital role in cardiovascular diseases. Receptor-interaction protein kinase 3- (RIPK3-) mediated necroptosis has crucially participated in cardiac dysfunction. The study is aimed at investigating the effect as well as the mechanism of CaMKII activation and necroptosis on diabetic cardiomyopathy (DCM). Wild-type (WT) and the RIPK3 gene knockout (RIPK3-/-) mice were intraperitoneally injected with 60 mg/kg/d streptozotocin (… Show more

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Cited by 19 publications
(24 citation statements)
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“…The inhibitor of necroptosis necrostatin-1 (nec-1) reduced visceral fat deposition and restored cognitive function and brain damage, but it did not result in any improvement on insulin sensitivity in prediabetic HFD rats ( Jinawong et al, 2020 ). RIPK3 deficiency alleviated myocardial injury, improved cardiac function, and attenuated necroptosis in mice with STZ-induced diabetic cardiomyopathy ( Chen et al, 2021 ). Our results suggest that necroptosis could be another pathway involved in kidney damage in diabetes to be explored.…”
Section: Discussionmentioning
confidence: 99%
“…The inhibitor of necroptosis necrostatin-1 (nec-1) reduced visceral fat deposition and restored cognitive function and brain damage, but it did not result in any improvement on insulin sensitivity in prediabetic HFD rats ( Jinawong et al, 2020 ). RIPK3 deficiency alleviated myocardial injury, improved cardiac function, and attenuated necroptosis in mice with STZ-induced diabetic cardiomyopathy ( Chen et al, 2021 ). Our results suggest that necroptosis could be another pathway involved in kidney damage in diabetes to be explored.…”
Section: Discussionmentioning
confidence: 99%
“…Some studies confirmed that myocardial cell necroptosis is observed in the hearts of diabetic patients and animal models ( 90 , 104 ). Recent studies described that activation of Ca2 + /calmodulin-dependent protein kinase (CaMKII) via a RIPK3-dependent manner or deficiency of sirtuin-3 (SIRT3) can exacerbate DCM through necroptosis enhancement in diabetic rats ( 105 , 106 ). Even so, direct evidence for the exact mechanism of necroptosis in DCM is not very clear and more in depth investigations are merited.…”
Section: Advance In Diabetic Cardiomyopathymentioning
confidence: 99%
“…These findings may open novel avenues for therapeutic strategies against diabetic cardiomyopathy. 78 …”
Section: Necroptosis In Human Diseases and Animal Modelsmentioning
confidence: 99%