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Related Experiment Video

Updated: Apr 29, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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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.

Free Radical Biology & Medicine
|April 27, 2026
PubMed

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Summary

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.
Keywords:
CalciumMitochondriaPyroptosisSICMSTIM1

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  • 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).