A double-edged sword: role of apoptosis repressor with caspase recruitment domain (ARC) in tumorigenesis and ischaemia/reperfusion (I/R) injury

Liu, Kun; Lan, Dongfeng; Li, Chunyang; Liu, Songpo; Dai, Xiaofang; Song, Tao; Xy, Wang; Kong, Qinghong; He, Zhixu; Tan, Jun; Zhang, Jidong

doi:10.1007/s10495-022-01802-4

Cited by 5 publications

(3 citation statements)

References 90 publications

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“…ARC is a recently discovered unique endogenous inhibitor of apoptosis with efficient and multifunctional effects. At present, research on the function of ARC mainly focuses on cancer and heart diseases, and studies show that ARC plays an anti-apoptotic role by regulating the interaction between ARC and caspase or its receptor proteins, including the specific inhibition of caspase-2 and caspase-8 activity 24 , 25 , which can antagonize apoptosis caused by hypoxia and so on 26 .…”

Section: Discussionmentioning

confidence: 99%

Effect of caspase inhibitors on hemodynamics and inflammatory factors in ARDS model rats

Liu,

Tian,

Zhou

et al. 2024

Sci Rep

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To study the effects of caspase inhibitors on hemodynamics and inflammatory factors in acute respiratory distress syndrome (ARDS) model rats. Sixty healthy male Wistar rats were randomly divided into three groups, namely, the control group, ARDS group and ARDS + Caspase inhibitor group, with 20 rats in each group. The control group was intraperitoneally injected with 2 mL/kg saline, and the ARDS model group was established by intraperitoneally injecting 4 mg/kg Lipopolysaccharide (LPS), ARDS + Caspase inhibitor group was adminstered 20 mg/kg caspase inhibitor after intraperitoneal LPS injection. Changes in pulmonary arterial pressure (PAP) and mean arterial pressure (MAP) at 6 and 12 h before and after administration were recorded. Moreover, arterial blood gas was evaluated with a blood gas analyzer and changes in the partial pressure of O2 (PaO2), partial pressure of CO2 (PaCO2), partial pressure of O2/fraction of inspired O2 (PaO2/FiO2) were evaluated. In addition, the lung wet/dry weight (W/D) ratio and inflammatory factor levels in lung tissue were determined. Finally, pathological sections were used to determine the pulmonary artery media thickness (MT), MT percentage (MT%), and the degree of muscle vascularization. The pulmonary arterial pressure of rats was determined at several time points. Compared with the control group, the model group had a significantly increased pulmonary arterial pressure at each time point (P < 0.01), and the mean arterial pressure significantly increased at 6 h (P < 0.05). Compared with that of rats in the model group, the pulmonary arterial pressure of rats in drug administration group was significantly reduced at each time point after administration (P < 0.01), and the mean arterial pressure was significantly reduced at 6 h (P < 0.05). The arterial blood gas analysis showed that compared with those in the control group, PaO2, PaCO2 and PaO2/FiO2 in the model group were significantly reduced (P < 0.01), and PaO2, PaCO2 and PaO2/FiO2 were significantly increased after caspase inhibitor treatment (P < 0.05 or 0.01). The levels of the inflammatory mediators tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in the model group were significantly higher than those in the control group (P < 0.01), and they were significantly decreased after caspase inhibitor treatment (P < 0.01). In the model group, pulmonary artery MT, MT% and the degree of muscle vascularization were significantly increased (P < 0.05 or 0.01), and pulmonary artery MT and the degree of muscle vascularization were significantly reduced after caspase inhibitor treatment (P < 0.05 or 0.01). Apoptosis Repressor with a Caspase Recuitment Domain (ARC) can alleviate the occurrence and development of pulmonary hypertension (PH) by affecting hemodynamics and reducing inflammation.

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Section: Discussionmentioning

confidence: 99%

Effect of caspase inhibitors on hemodynamics and inflammatory factors in ARDS model rats

Liu,

Tian,

Zhou

et al. 2024

Sci Rep

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“…Widely studied RCDs in heart disease includes apoptosis, necroptosis, and autophagy. 4 , 5 , 6 Ferroptosis, a recently added RCD member, is a non-apoptotic form of RCD caused by excessive production of lipid hydroperoxides in the presence of iron. 7 Ferroptotic cells do not demonstrate apoptotic hallmarks such as caspase activation or cell blebbing.…”

Section: Introductionmentioning

confidence: 99%

Cardiomyocyte-fibroblast interaction regulates ferroptosis and fibrosis after myocardial injury

Mohr,

Li,

Trouten

et al. 2024

iScience

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“…It is unclear to what extent each type of RCDs contributes to the loss of cardiomyocytes in the infarcted myocardium. Widely studied RCDs in heart disease includes apoptosis, necroptosis, and autophagy [4][5][6] . Ferroptosis, a recently added RCD member, is a non-apoptotic form of RCD caused by excessive production of lipid hydroperoxides in the presence of iron 7 .…”

Section: Introductionmentioning

confidence: 99%

Cardiomyocyte-fibroblast interaction regulates ferroptosis and fibrosis after myocardial injury

Mohr

Trouten

et al. 2023

Preprint

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Neonatal mouse hearts have transient renewal capacity which is lost in juvenile and adult hearts. After myocardial infarction (MI) in neonatal hearts, an initial loss of cardiomyocytes occurs but it is unclear through which type of regulated cell death (RCD). In the current studies, we induced MI in neonatal and juvenile mouse hearts, and show that ischemic cardiomyocytes primarily undergo ferroptosis, a non-apoptotic and iron-dependent form of RCD. We demonstrate that cardiac fibroblasts (CFs) protect cardiomyocytes from ferroptosis through paracrine factors and direct cell-cell interaction. CFs show strong resistance to ferroptosis due to high ferritin expression. Meanwhile, the fibrogenic role of CFs, typically considered detrimental to heart function, is negatively regulated by paired-like homeodomain 2 (Pitx2) signaling from cardiomyocytes. In addition, Pitx2 prevents ferroptosis in cardiomyocytes by regulating ferroptotic genes. Understanding the regulatory mechanisms of cardiomyocyte survival and death can identify potentially translatable therapeutic strategies for MI.

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A double-edged sword: role of apoptosis repressor with caspase recruitment domain (ARC) in tumorigenesis and ischaemia/reperfusion (I/R) injury

Cited by 5 publications

References 90 publications

Effect of caspase inhibitors on hemodynamics and inflammatory factors in ARDS model rats

Effect of caspase inhibitors on hemodynamics and inflammatory factors in ARDS model rats

Cardiomyocyte-fibroblast interaction regulates ferroptosis and fibrosis after myocardial injury

Cardiomyocyte-fibroblast interaction regulates ferroptosis and fibrosis after myocardial injury

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