Table 1. Brief observation of articles included in this review.

H₂S, hydrogen sulfide; UUO, unilateral ureteral obstruction; HSCs, hepatic stellate cells; CCl₄, carbon tetrachloride; ECM, extracellular matrix; EMT, endothelial-to-mesenchymal transition; α-SMA, α-smooth muscle actin; RAAS, renin–angiotensin–aldosterone system

Author	Conclusion
Renal fibrosis
Dugbartey [11]	H2S restores oxygen mechanism and increases medullary blood flow.
Han et al. [13]	H2S deficiency leads to fibrosis.
Wang et al. [14]	H2S resulted in improved vascular remodeling and high blood pressure.
Qian et al. [15]	Reduced endogenous H2S contributes to diabetic injury; exogenous H2S protects tissues from diabetic damage.
Sun et al. [16]	The H2S signaling pathway is involved in the treatment of diabetic nephropathy.
Lin et al. [17]	H2S donor molecules led to significant decreases in inflammation, fibrosis, and the expression of epithelial–mesenchymal transition markers following urinary obstruction.
Jiang et al. [18]	Sodium hydrosulfide protects against UUO-induced renal damage.
Dursun et al. [19]	H2S has preventive effect on UUO-induced kidney damage in rats by reducing oxidative stress.
Lee et al. [20]	Aging-induced kidney changes are alleviated following H2S administration by inhibiting signaling pathways leading to matrix protein synthesis.
Hepatic fibrosis
Song et al. [12]	The metabolic levels of H2S and its producing enzymes were recorded to change in hepatic fibrosis.
Mani et al. [22]	Hepatic H2S metabolism’s malfunction may be involved in many liver diseases.
Fan et al. [23]	Exogenous H2S inhibits proliferation and induces cell cycle arrest and apoptosis in activated HSCs and attenuates CCl4-induced hepatic fibrosis and ECM gene expression.
Zhang et al. [24]	Diallyl trisulfide hinders pro-fibrogenic properties and reduces oxidative stress by an H2S-associated mechanism in HSCs.
Myocardial fibrosis
Ying et al. [29]	H2S could protect against endoplasmic reticulum stress-induced EMT through the Src pathway.
Snijder et al. [30]	H2S causes a reduction in fibronectin and galectin‐3, the inhibition of which prevents cardiac remodeling by interfering with myocardial fibrogenesis.
Shen et al. [31]	H2S exhibits angiogenic and anti-inflammatory actions; it also preserves mitochondrial function and reduces apoptosis.
Sheng et al. [32]	H2S suppresses potassium channel activity, attenuating atrial fibroblast proliferation and differentiation toward myofibroblasts.
Lilyanna et al. [33]	GYY4137, a slow-releasing H2S donor, cause enhanced early postischemic endogenous natriuretic peptide activation; it may also exert postischemic cardioprotective effects.
Meng et al. [34]	GYY4137 inhibits oxidative stress, blocks the TGF-β1/Smad2 signaling pathway, and decreases the expression of α-SMA.
Pan et al. [35]	Exogenous H2S prevented cardiac remodeling through ECM accumulation inhibition and increased vascular density.
Tran et al. [41]	Liposomal formulations, which release H2S slowly within tissues, have exhibited enhanced cardioprotective effects in vivo via the inhibition of the TGF-β1/Smad signaling pathway.
Song et al. [12]	H2S inhibits the local RAAS.
Pulmonary fibrosis
Chen et al. [42]	H2S metabolism in the lungs is associated with respiratory diseases.
Zhang et al. [7]	A decrease in H2S-producing enzymes and endogenous H2S levels is associated with pulmonary fibrosis development.
Bazhanov et al. [43]	Endogenous H2S in the respiratory tract regulates essential functions.