Abstract
Harmful, stressful conditions or events in the cardiovascular system result in cellular damage, inflammation, and fibrosis. Currently, there is no targeted therapy for myocardial fibrosis, which is highly associated with a large number of cardiovascular diseases and can lead to fatal heart failure. Hydrogen sulfide (H(2)S) is an endogenous gasotransmitter similar to nitric oxide and carbon monoxide. H(2)S is involved in the suppression of oxidative stress, inflammation, and cellular death in the cardiovascular system. The level of H(2)S in the body can be boosted by stimulating its synthesis or supplying it exogenously with a simple H(2)S donor with a rapid- or slow-releasing mode, an organosulfur compound, or a hybrid with known drugs (e.g., aspirin). Hypertension, myocardial infarction, and inflammation are exaggerated when H(2)S is reduced. In addition, the exogenous delivery of H(2)S mitigates myocardial fibrosis caused by various pathological conditions, such as a myocardial infarct, hypertension, diabetes, or excessive β-adrenergic stimulation, via its involvement in a variety of signaling pathways. Numerous experimental findings suggest that H(2)S may work as a potential alternative for the management of myocardial fibrosis. In this review, the antifibrosis role of H(2)S is briefly addressed in order to gain insight into the development of novel strategies for the treatment of myocardial fibrosis.