Table 1.

Comparison of different forms of cell death and their biological features.

Mode	Object of study	Intervention mode	Conclusion	Ref
A	Mice	Melatonin	Melatonin protects against sepsis-induced cardiac dysfunction by regulating apoptosis and autophagy via activation of SIRT1 in mice.	[49]
A	Septic mice	TMZ	TMZ protected against LPS-induced myocardial dysfunction and apoptosis, accompanied by inhibition of macrophage pro-inflammatory responses.	[50]
P	Mice	TMZ	TMZ as a potential therapeutic agent for septic or endotoxemia-associated cardiac dysfunction in mice.	[45]
A	Rats	miR-25	miR-25 inhibits sepsis-induced cardiomyocyte apoptosis by targeting PTEN.	[51]
A	Septic rats	AC2-26	AC2-26 may alleviate the sepsis-induced cardiomyocyte apoptosis in vivo and in vivo through the LXA4/PI3K/AKT signaling pathway.	[52]
A	Septic rats	Calpain inhibitors	Akt/eNOS/NO pathway might lead to a novel pharmacological therapy for cardiomyocytes apoptosis in sepsis.	[53]
A	Septic rats	Esmolol	Esmolol reduces apoptosis and inflammation in early sepsis rats with abdominal infection.	[54]
P and A	Mice	Stimulator of interferon genes	STING-IRF3 contributes to LPS-induced cardiac dysfunction, inflammation, apoptosis, and pyroptosis by activating NLRP3.	[55]
P	HCM cells	Angiotensin II	miR-133a-3p upregulation may be a promising strategy for cardiac hypertrophy treatment.	[56]
P	H9C2 rat cardiomyoblast cell	LPS	LPS aggravates high glucose- and hypoxia/reoxygenation-induced injury through activating ROS-dependent NLRP3 inflammasome-mediated pyroptosis in H9C2 cardiomyocytes.	[57]
P	Septic BALB/c mice	Thymoquinone	Role of thymoquinone in cardiac damage caused by sepsis from BALB/c mice.	[58]
P	LPS-treated mice	Geniposide	Geniposide protects against sepsis-induced myocardial dysfunction through the AMPKα-dependent pathway.	[59]
P	A mouse hyperuricemia model	IR (MI/R)	UA aggravates MI/R-induced activation of the NLRP3 inflammatory cascade and pyroptosis by promoting ROS generation, while inflammasome inhibitors and ROS scavengers partly reverse the injury.	[60]
P	LPS-induced mice/CORM-3-treated mice	CO-releasing molecule-3	Carbon monoxide releasing molecule-3 improves myocardial function in mice with sepsis by inhibiting NLRP3 inflammasome activation in cardiac fibroblasts.	[61]
N	Mice lacking CypD	CypD-deficient mice by gene targeting	The CypD-dependent mPT regulates some forms of necrotic death, but not apoptotic death.	[10]
N	Mouse	CypD or RIP3 knockout	RIP3–CaMKII–MPTP myocardial necroptosis pathway, a promising target for the treatment of ischemia- and oxidative stress-induced myocardial damage and heart failure.	[62]
N	Heart failure patients	Detection of the level of death receptor	Necrosis-related factor and miR-873 can regulate programmed necrosis in the heart.	[63]
Au	Domestic swine	IR (MI/R)	Autophagy, triggered by ischemia, could be a homeostatic mechanism, by which apoptosis is inhibited and the deleterious effects of chronic ischemia are limited.	[35]
Au	Sepsis-induced rats	Melatonin	The study sheds light on the important role of Beclin-1 acetylation in regulating autophagy in sepsis and suggests that melatonin is a potential candidate drug for the treatment of sepsis.	[64]
Au	H9C2 rat cardiomyoblast cell	Hypoxia/reoxygenation (H/R)	miR-542-5p/autophagy pathway might be a potential target for the treatment of H/R-related heart diseases.	[65]

A: Apoptosis; Au: Autophagy; CypD: Cyclophilin D; IR: Ischemia-reperfusion; LPS: Lipopolysaccharides; MPTP: Mitochondrial permeability transition pore; N: Necrosis; NLRP3: Nucleotide-binding oligomerization domain-like receptor protein 3; P: Pyroptosis; ROS: Reactive oxygen species; TMZ: Trimetazidine; AC2-26: an active N-terminal peptide of AnxA1(Annexin A1); MI/R: Myocardial ischemia reperfusion; CO: Carbon monoxide; mPT: Mitochondrial permeability transition; RIP3:Receptor-interacting serine-threonine kinase 3.