Table 1.

Apoptotic regulators associated with ischemic-reperfusion injury that are responsive to hydrogen sulfide

H2S target	Cell/tissue type	Functions	References
Akt	Cardiac, renal, neural, hepatic	JNK, mTOR, GSK3β, NR2A and B activation	[32, 42, 93, 101, 117]
HSP	Retinal, hepatic	Thioredoxin-1 activation, ROS scavenging, reducing inflammatory cytokine induction	[93, 94, 102]
JNK	Cardiac, retinal, renal, hepatic, epithelial	Bcl-2 inactivation, cytochrome C release	[90, 94, 118, 119]
Beclin-1	Cardiac, hepatic	Decrease autophagosome formation	[39, 99]
GSK3β	Cardiac, hepatic, neural	Activate Bax, decrease LC3 and Beclin-1, inhibit mPTP opening,	[6, 72, 95, 101]
Bcl-2	Cardiac, renal, hepatic, neural, epithelial	Prevent cytochrome C release, inactivate Bax	[72, 91, 95, 99, 101, 102, 105]
TNFα, IL-6, IL-1β	Cardiac, skeletal muscle, lung	ROS increase, mPTP opening, Bax activation	[24, 99, 106–109, 118]
miRNA (1, 21, 485-5p)	Cardiac, neural	Reduce LDH, regulate transcriptional activation, reduce TNFα activity	[114–116]