Role of copper ion overload triggered by CD44 endocytosis on STAT3-mediated cuproptosis in septic myocardial injury DOI
Meng Zhang,

Donglin Fu,

Qiuhong Zhang

et al.

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: May 7, 2025

Abstract Sepsis-induced myocardial injury (SIMI) is a severe complication in sepsis patients, contributing to high mortality rates. The pathogenesis remains unclear, but emerging evidence suggests copper ion overload may trigger cell death via "cuproptosis." This study investigates the role of CD44, glycoprotein involved inflammation and metal uptake, copper-induced SIMI. Using an LPS-induced H9C2 cardiomyocyte model, we found CD44 expression upregulated SIMI, correlating with increased levels oxidative stress. inhibition reduced mitigated damage, confirming its copper-mediated injury. Furthermore, facilitated uptake into mitochondria, inducing dysfunction STAT3 pathway activation. overexpression exacerbated injury, highlighting critical role. These findings suggest CD44-mediated activation contributes positioning as potential therapeutic strategy for sepsis-induced damage.

Language: Английский

Role of copper ion overload triggered by CD44 endocytosis on STAT3-mediated cuproptosis in septic myocardial injury DOI
Meng Zhang,

Donglin Fu,

Qiuhong Zhang

et al.

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: May 7, 2025

Abstract Sepsis-induced myocardial injury (SIMI) is a severe complication in sepsis patients, contributing to high mortality rates. The pathogenesis remains unclear, but emerging evidence suggests copper ion overload may trigger cell death via "cuproptosis." This study investigates the role of CD44, glycoprotein involved inflammation and metal uptake, copper-induced SIMI. Using an LPS-induced H9C2 cardiomyocyte model, we found CD44 expression upregulated SIMI, correlating with increased levels oxidative stress. inhibition reduced mitigated damage, confirming its copper-mediated injury. Furthermore, facilitated uptake into mitochondria, inducing dysfunction STAT3 pathway activation. overexpression exacerbated injury, highlighting critical role. These findings suggest CD44-mediated activation contributes positioning as potential therapeutic strategy for sepsis-induced damage.

Language: Английский

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