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Table 1 Apoptotic regulators associated with ischemic-reperfusion injury that are responsive to hydrogen sulfide

From: Mechanisms by which hydrogen sulfide attenuates muscle function following ischemia–reperfusion injury: effects on Akt signaling, mitochondrial function, and apoptosis

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, 106,107,108,109, 118]

miRNA (1, 21, 485-5p)

Cardiac, neural

Reduce LDH, regulate transcriptional activation, reduce TNFα activity

[114,115,116]