Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac inflammation and heart failure development.

ABSTRACT: Inflammation promotes heart failure (HF) development, and inhibition of IL-12β simultaneously attenuates interleukin-12 (IL-12) and interleukin-23 (IL-23), two important proinflammatory cytokines. In this study, we used IL-12β knockout (KO) mice to test the hypothesis that genetic inhibition of IL-12β would attenuate transverse aortic constriction (TAC)-induced cardiac inflammation, hypertrophy, and dysfunction, as well as the consequent lung remodeling. IL-12β KO in male and female mice significantly attenuated TAC-induced cardiac dysfunction as evidenced by improved left ventricular (LV) ejection fraction and fractional shortening. IL-12β KO also significantly ameliorated the TAC-induced increase of LV weight, left atrial weight, lung weight, right ventricular (RV) weight, and their rati

SUBMITTER: Bhattarai U 

PROVIDER: S-EPMC12439980 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature