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Targeting STIM1 attenuates LPS-induced cardiac dysfunction by reshaping calcium homeostasis and mitochondrial
Qing-Rui Wu1, Li-Bo Luo2, Hui Yang3
1Guangdong Provincial Key Laboratory of Clinical Pharmacology, Research Center of Medical Sciences, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, 510080, Guangzhou, Guangdong, China; State Key Laboratory of Respiratory Disease, Institute of Pulmonary Diseases, Department of Critical Care Medicine, Guangzhou Chest Hospital, Guangzhou Medical University, Guangzhou, 510095, China.
STIM1 protein upregulation worsens sepsis-induced cardiomyopathy (SICM) by disrupting calcium handling and mitochondrial function. Targeting STIM1 offers a potential therapeutic strategy for SICM.
Area of Science:
- Cardiology
- Molecular Biology
- Cellular Biology
Background:
- Sepsis-induced cardiomyopathy (SICM) involves disrupted calcium homeostasis and mitochondrial dysfunction.
- Stromal interaction molecule 1 (STIM1) plays a key role in calcium regulation.
- The specific role of STIM1 in SICM pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the role and mechanism of STIM1 in sepsis-induced cardiomyopathy (SICM).
- To determine if modulating STIM1-mediated calcium handling can alleviate SICM.
Main Methods:
- Established a rat model of sepsis using lipopolysaccharide (LPS).
- Utilized myocardial-specific STIM1 knockdown in septic rats.
- Employed the calcium influx inhibitor BTP2.
- Investigated STIM1's mechanism in LPS-treated cardiomyocytes.
Main Results:
- STIM1 protein was upregulated in sepsis-induced cardiomyopathy (SICM).
- STIM1 knockdown improved cardiac function in septic rats.
- BTP2 alleviated LPS-induced cardiomyopathy by enhancing calcium and mitochondrial function.
- STIM1 amplifies calcium entry, leading to overload, mitochondrial fragmentation, ROS production, and NLRP3 inflammasome-mediated pyroptosis.
Conclusions:
- STIM1 promotes SICM by exacerbating calcium overload, mitochondrial dysfunction, and cardiomyocyte pyroptosis.
- Targeting STIM1 presents a promising therapeutic avenue for treating sepsis-induced cardiomyopathy (SICM).
