Abstract
Sepsis-induced cardiac injury (SIC) is one of the most common complications in the intensive care unit (ICU) with high morbidity and mortality. Mitochondrial dysfunction is one of the main reasons for SIC, and Interleukin-13 (IL-13) is a master regulator of mitochondria biogenesis. The aim of the present study was to investigate the role of IL-13 in SIC and explore the underlying mechanism. It was found that reactive oxygen species (ROS) production and apoptosis were significantly increased in lipopolysaccharide (LPS)-stimulated primary cardiomyocytes, which was accompanied with obvious mitochondria dysfunction. The results of RNA-sequencing (RNA-seq), mitochondrial membrane potential, fatty acid uptake and oxidation rate suggested that treatment with IL-13 could restore the function and morphology of mitochondria, indicating that it played an important role in protecting septic cardiomyocytes. These findings demonstrated that IL-13 alleviated sepsis-induced cardiac inflammation and apoptosis by improving mitochondrial fatty acid uptake and oxidation, suggesting that IL-13 may prove to be a potential promising target for SIC treatment.
Highlights
Sepsis-induced myocardial dysfunction is one of the main causes of death in the intensive care unit (ICU)
We explored the therapeutic effect of IL-13 with primary cardiomyocytes
Numerous mechanisms including calcium overload, reactive oxygen species (ROS) production, calcium overload, inactivation of ion channels and mitochondria dysfunction are involved in the development of Sepsis-induced cardiac injury (SIC)
Summary
Sepsis-induced myocardial dysfunction is one of the main causes of death in the intensive care unit (ICU). Various theories and therapies have been proposed to treat septic patients with impaired cardiac function (Ichinose et al, 2007; Xu et al, 2012; Venet and Monneret, 2018). Mitochondrial dysfunction has been considered as a crucial cause of sepsis-induced cardiac injury (SIC) with augmented release of reactive oxygen species (ROS) and decreased mitochondrial oxidative phosphorylation (Drosatos et al, 2011, 2013; Schilling et al, 2011). Toxic ROS and insufficient energy metabolism lead to the impairment and apoptosis of cardiomyocytes (Sepúlveda et al, 2020). IL-13 is reported to be increased after endurance exercise, probably due to type 2 innate lymphocytes (ILC2) expansion
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