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Interleukin (IL)-10 cytokine family members, including IL-10, IL-19, IL-20, IL-22, IL-24, IL-26 and the distantly related IL-28A, IL-28B, and IL-29, play critical roles in the regulation of inflammation. The occurrence and progression of cardiovascular diseases closely correlate with the regulation of inflammation, which may provide novel strategies for the treatment of cardiovascular diseases. In recent years, studies have focused on the association between the IL-10 cytokine family and the physiological and pathological progression of cardiovascular diseases. The aim of this review is to summarize relevant studies and clarify whether the IL-10 cytokine family contributes to the regulation of cardiovascular diseases.

Activation of the NLRP3 inflammasome promotes pathological cardiac remodeling induced by pressure overload. However, the therapeutic effects of NLRP3 inhibition after cardiac remodeling remain unknown. The present study aimed to investigate whether the selective NLRP3 inhibitor, MCC950, could reverse transverse aortic constriction (TAC)-induced cardiac remodeling. Mice were divided into four groups based on the treatment given: sham, sham + MCC950, TAC, and TAC + MCC950. MCC950 (10 mg/kg, intraperitoneal injection, once per day) was administered from two weeks after TAC or sham surgery for four weeks. Echocardiography, histological analysis, RT-PCR, and Western blotting were performed to explore the function of MCC950 after TAC. We found that MCC950 reversed cardiac dysfunction after TAC. MCC950 attenuated cardiac hypertrophy by down-regulating calcineurin expression and inhibiting MAPK activation. Further, it also alleviated cardiac fibrosis post-TAC by inhibiting the TGF-β/Smad4 pathway, and reduced cardiac inflammation and macrophage infiltration post-TAC, including both M1 and M2 macrophages. Taken together, MCC950 can attenuate cardiac remodeling due to pressure overload by inhibiting hypertrophy, fibrosis, and inflammation. Our study provides a basis for the clinical application of NLRP3 inhibitors in the treatment of non-ischemic heart failure.