Table 2.
Effects of Endogenous H2S and Exogenous H2S in AS.
| Source | Gene/Compound | Effects | Mechanism | Reference |
|---|---|---|---|---|
| Endogenous | CSE | CSE deficiency upregulated the levels of IL-1β and IL-18 inflammatory cytokines | Via activating TXNIP-NLRP3-IL-18/IL-1β-NO signaling pathway | (47) |
| CSE depletion contributes to the development of endothelial dysfunction in AS | Via activating MAPK/TXNIP pathway | (48) | ||
| protective against the formation of uremia accelerated atherosclerosis | Via activating eNOS/PKC βII/Akt signaling pathway | (49) | ||
| reducing atherosclerotic plaque formation, by reducing vascular related inflammation | sulfhydrate SIRT1, promote its deacetylation activity, and increase SIRT1 stability | (59) | ||
| anti-inflammatory role in ox-LDL-stimulated macrophage | suppressing JNK/NF-κB signaling pathway | (58) | ||
| Exogenous | NaHS | protective in endothelial cells | upregulating ACE2 expression | (51) |
| NaHS | reverse the endothelial dysfunction induced by AngII in HUVECs | via ER stress pathway | (52) | |
| NaHS | improve vascular function by reducing vascular superoxide generation and impairing atherosclerotic lesion development | reducing endothelial dysfunction and inhibiting vascular superoxide generation | (54) | |
| GYY4137 | reducing oxidant-provoked vascular endothelial dysfunction | upregulate activator protein 1 activity with the SIRT3 promoter | (53) | |
| GYY4137 | protect endothelial cells from Ox-LDL-induced apoptosis by activating Sirt1 | induce autophagy | (55) | |
| GYY4137 | inhibit lipopolysaccharide -induced release of pro-inflammatory mediators and promoted the release of the anti-inflammatory chemokines | Not applicable | (65) | |
| GYY4137 | be protective against the development of diabetes-accelerated AS | preventing the activation of NLPR3 inflammasome | (66) | |
| AP39 and AP123 | protect endothelial cells from highglycemia-induced injury | preserving mitochondria function | (56) | |
| zofenoprilat | exert anti-inflammatory activity in vascular cells | In a CSE/H2S-mediated manner | (60) |
CSE, cystathionine-c-lyase; NO, nitric oxide; TXNIP, thioredoxin-interacting protein; NLPR3, Nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3; NO, nitric oxide; MAPK, mitogen-activated protein kinase; eNOS, endothelial nitric oxide synthase; PKC, protein kinase C; SIRT, Sirtuin; ox-LDL, oxidized low-density lipoprotein; JNK, c-Jun N-terminal kinase; ACE2, angiotensin converting enzyme 2; ER, endoplasmic reticulum; HUVEC, human umbilical vein endothelial cell.