Table 1.

The anticancer drugs-caused cardiac injury was antagonized by H₂S.

Drug/class of drugs	Cardiac toxic effect limited by H2S	Mechanism of action
Adriamycin (Su et al., 2009)	H2S improves the impairment of cardiac function and alleviates the cardiac pathological change in adriamycin-treated rats.	Reduces lipid peroxidation, increases the activities of antioxidant enzyme, and therefore inhibits oxidative stress injury.
Doxorubicin (Wang et al., 2012)	H2S improves cellular survival in the doxorubicin-treated H9c2 cardiac cells.	Inhibits the endoplasmic reticulum stress.
Doxorubicin (Guo et al., 2013a)	H2S attenuates the doxorubicin-induced inflammation and cytotoxicity in H9c2 cardiac cells.	Depresses the p38 MAPK/NF-κB pathway.
Doxorubicin (Guo et al., 2013b)	H2S protects against doxorubicin-induced cytotoxicity, apoptosis, mitochondrial damage and oxidative stress in H9c2 cardiac cells.	Inhibits the p38 MAPK pathway.
Doxorubicin (Liu et al., 2015a,b, 2016a,b)	H2S protects against doxorubicin-induced cytotoxicity and apoptosis in H9c2 cardiac cells.	1. Inhibits calreticulin expression. 2. Suppresses reactive oxygen species-activated extracellular signal-regulated kinase 1/2 pathway. 3. Restores the imbalance between anti-apoptotic protein bcl-2 and pro-apoptotic protein bax. 4. Inhibits peroxiredoxin III expression. 5. Activates PI3K/Akt pathway, enhances the phosphorylation of FoxO3a and then reduces the nuclear translocation of FoxO3a.
Doxorubicin (Yu et al., 2017)	H2S protects against doxorubicin-induced dilated cardiomyopathy in rats.	1. Activates Nrf2 signaling to reduce doxorubicin-induced oxidative stress. 2. Activates PI3K/Akt pathway to exert antiapoptotic effects.
Doxorubicin (Zhang et al., 2011)	S-diclofenac, a novel H2S-releasing derivative of diclofenac, significantly ameliorates doxorubicin-related cardiac injury and cardiac dysfunction, and improves the survival rate of mice with doxorubicin-induced cardiomyopathy.	1. Reverses the cardiac gap junction remodeling via suppressing the activation of JNK pathway. 2. Inhibits the oxidative stress and inflammation in the mouse heart.
Doxorubicin (Chegaev et al., 2016)	H2S-DOXO, an H2S releasing DOXO derivative, protects against DOXO-induced cytotoxicity in H9c2 cardiac cells.	Reduces the amount of ROS produced by DOXO.
Doxorubicin (Wu et al., 2016)	SPRC, a producing agent of endogenous H2S, prevents doxorubicin-induced cardiac cytotoxicity in vitro and in vivo.	Activates the gp130/STAT3 pathway, and then inhibits apoptosis and oxidative stress, finally leads to antagonizing mitochondrial dysfunction and intracellular Ca2+ overload in the doxorubicin-treated mice and H9c2 cells.