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. 2020 May 16;27:85–97. doi: 10.1016/j.jare.2020.05.007

Table 2.

Effects of H2S on proliferation and apoptosis of vascular smooth muscle cells.

Action Mechanisms Cells/Models H2S gas/donor application (concentration) Refs.
Anti-proliferation Inhibition of Brg1 transcription and expression by reducing the recruitment of Brg1 to the Pcna, Ntf3 and Pdgfα promoter regions VSMCs NaHS (1000 μM) [59]
Anti-proliferation Inhibition of the MAPK pathway VSMC isolated from rat thoracic aortas NaHS (50–500 μM) [57]
Anti-proliferation Inhibition of the MAPK/TXNIP cascade HUVECs/CSE-KO mice NaHS (56 µM/kg/d) [58]
Anti-proliferation Inhibition of the expression of IGF-1R and the binding of IGF-1 with IGF-1R via S-sulfhydration SMCs isolated from mouse mesenteric arteries NaHS (10–100 μM) [60]
Inducing apoptosis/Anti-proliferation Increasing ERK1/2, p21Cip/WAF-1, and decreasing cyclin D1 in SMCs-KO mice.
Inhibition of proliferation-related genes CRL, HB-EGF and IB1 in CSE KO mice.
SMCs-KO mice/CSE-KO mice/HASMCs H2S (100 μM) [56], [62]
Inducing apoptosis Activation of MAPKs and caspase-3 HASMCs H2S (50–100 μM) [63]
Inhibiting apoptosis Activation of SOD activity
Inhibition of ROS generation and MDA levels
HUVECs NaHS (50 μM) [64]
Inhibiting apoptosis Inhibition of caspase-12, CHOP, GRP78 PAECs NaHS (56 µM/kg/d) [65]