Abstract

Hydrogen sulfide (H2S) has been recognized as the third gasotransmitter, following nitric oxide and carbon monoxide, and it exerts important biological effects in the body. Growing evidence has shown that H2S is involved in many physiological processes in the body. In recent years, much research has been carried out on the role of H2S in bone metabolism. Bone metabolic diseases have been linked to abnormal endogenous H2S functions and metabolism. It has been found that H2S plays an important role in the regulation of bone diseases such as osteoporosis and osteoarthritis. Regulation of H2S on bone metabolism has many interacting signaling pathways at the molecular level, which play an important role in bone formation and absorption. H2S releasing agents (donors) have achieved significant effects in the treatment of metabolic bone diseases such as osteoporosis and osteoarthritis. In addition, H2S donors and related drugs have been widely used as research tools in basic biomedical research and may be explored as potential therapeutic agents in the future. Donors are used to study the mechanism and function of H2S as they release H2S through different mechanisms. Although H2S releasers have biological activity, their function can be inconsistent. Additionally, donors have different H2S release capabilities, which could lead to different effects. Side effects may form with the formation of H2S; however, it is unclear whether these side effects affect the biological effects of H2S. Therefore, it is necessary to study H2S donors in detail. In this review, we summarize the current information about H2S donors related to bone metabolism diseases and discuss some mechanisms and biological applications.

Highlights

  • With the development of aging society, the incidence of bone metabolic diseases is increasing year by year, such as osteoporosis and osteoarthritis, which seriously affects the quality of life of the elderly

  • Promote osteoblast proliferation Protect osteoblasts from oxidative stress-induced cell damage Stimulate the transcription level of osteocalcin Prevent DEX-induced bone loss, stimulate the formation and differentiation of osteoblasts Protect osteoblasts from Reactive oxygen species (ROS) formation Increases the activity of alkaline phosphatase and Ca2+ ATPase Anti-inflammation and inhibit bone defects and bone loss

  • GYY4137 protected osteoblasts from apoptosis induced by DEX. These results indicate that GYY4137 is an effective way to prevent and treat osteoporosis and osteonecrosis caused by glucocorticoids (GCs) (Ma et al, 2019)

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Summary

Introduction

With the development of aging society, the incidence of bone metabolic diseases is increasing year by year, such as osteoporosis and osteoarthritis, which seriously affects the quality of life of the elderly. H2S protects osteoblasts from oxidative stress-induced cell damage and proliferation and differentiation inhibition through mitogen-activated protein kinase (MAPK) (P38 and ERK1/2)-dependent mechanisms; H2S may have potential therapeutic value for

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