Sepsis-induced myocardial dysfunction:novel therapeutic perspectives focusing on immunometabolism and cell death mechanisms
Liu Yuan
Mei Jianqiang
Abstract：Sepsis-induced myocardial dysfunction(SIMD)is a critical independent risk factor for mortality in patients with sepsis,yet its complex pathogenesis and the lack of specific treatments remain major clinical challenges.Existing research reveals that the pathogenesis of SIMD is closely associated with a vicious cycle network formed by dysregulated immune recognition-dysfunctional metabolic reprogramming-activation of programmed cell death.This review synthesizes current knowledge on the molecular mechanisms underlying the interaction between immunometabolic disturbances and various forms of cell death in SIMD,focusing on the synergistic damaging effects of pyroptosis and ferroptosis.It also reviews preclinical evidence and translational prospects for novel therapeutic strategies targeting the nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome,ferroptosis pathways,mitochondrial function,and sodium-glucose cotransporter 2(SGLT2)inhibitors.Furthermore,by integrating advances in novel circulating biomarkers such as soluble suppression of tumorigenicity 2(sST2)and growth differentiation factor-15(GDF-15),and imaging techniques like speckle tracking echocardiography(STE),this article explores future directions for precise phenotyping and personalized therapy of SIMD.Targeted intervention in the immunity-metabolism-cell death network offers a promising framework for overcoming the therapeutic impasse in SIMD,providing new theoretical foundations and potential clinical strategies.
Keywords：Sepsis-induced myocardial dysfunctionImmunometabolismRegulated cell deathNucleotide-binding oligomerization domain-like receptor protein 3 inflammasomeFerroptosis
Publication Date：2026-03-10
Online Publishing Date：2026-03-27(First online date of this platform, not the publication date of the document)
Pages：5( 176-180 )