Sepsis‑induced cardiac dysfunction is one of the most common types of organ dysfunction in sepsis; its pathogenesis is highly complex and not yet fully understood. Cardiomyocytes serve a key role in the pathophysiology of cardiac function; due to the limited ability of cardiomyocytes to regenerate, their loss contributes to decreased cardiac function. The activation of inflammatory signalling pathways affects cardiomyocyte function and modes of cardiomyocyte death in sepsis. Prevention of cardiomyocyte death is an important therapeutic strategy for sepsis‑induced cardiac dysfunction. Thus, understanding the signalling pathways that activate cardiomyocyte death and cross‑regulation between death modes are key to finding therapeutic targets. The present review focused on advances in understanding of sepsis‑induced cardiomyocyte death pathways, including apoptosis, necroptosis, mitochondria‑mediated necrosis, pyroptosis, ferroptosis and autophagy. The present review summarizes the effect of inflammatory activation on cardiomyocyte death mechanisms, the diversity of regulatory mechanisms and cross‑regulation between death modes and the effect on cardiac function in sepsis to provide a theoretical basis for treatment of sepsis‑induced cardiac dysfunction.

Infectious diseases, especially sepsis from bacterial infections, significantly threaten global health, with antimicrobial resistance (AMR) complicating treatment and increasing clinical burdens. Antibiotic overuse contributes to AMR by creating selective pressure, reducing the efficacy of traditional therapies, and necessitating new approaches. Endogenous hydrogen sulfide (H₂S), a gaseous signaling molecule produced by most bacteria through cystathionine-γ-lyase (CSE), cystathionine-β-synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3MST), plays a crucial role in bacterial resistance. This review explores the biological functions of bacterial endogenous H₂S and its impact on AMR. H₂S enhances resistance by neutralizing antibiotic-induced reactive oxygen species (ROS), reducing oxidative stress and DNA damage, and promoting biofilm formation, which obstructs antibiotic penetration and facilitates resistance gene exchange. Furthermore, enhancing H₂S-based assays could significantly improve the diagnosis of AMR. Additionally, strategies such as targeting H₂S metabolism—through the use of H₂S synthase inhibitors or disrupting biofilms via H₂S clearance—or the combination of H₂S synthase inhibitors with antibiotics, may reverse resistance. A deeper understanding of the mechanisms by which H₂S mediates resistance is essential for the development of advanced diagnostic tools and innovative therapies to combat AMR. Its clinical translation may reverse AMR passivity, guide antibiotic sensitizer development, and optimize therapies, holding significant clinical and translational value.