Tongxinluo prevents chronic obstructive pulmonary disease complicated with atherosclerosis by inhibiting ferroptosis and protecting against pulmonary microvascular barrier dysfunction

Wang, Ya-Fen; Kuang, Xiangnan; Yin, Yuehui; Han, Ningxin; Chang, Liping; Wang, Hongtao; Hou, Yunlong; Li, Huixin; Li, Zhen; Liu, Yi; Hao, Yuanjie; Wei, Yaru; Wang, Xiaoqi; Jia, Zhenhua

doi:10.1016/j.biopha.2021.112367

Cited by 33 publications

(20 citation statements)

References 65 publications

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“…When the damage of Hcy to ECs is further aggravated, the cells may go toward death, resulting in severe endometrial damage. Numerous studies have shown that Hcy can cause various forms of ECs death, such as apoptosis ( 75 ), pyroptosis ( 76 ), and ferroptosis ( 77 ). Pyroptosis is a newly discovered form of programed cell death, which depends on gasdermin family proteins such as gasdermin D (GSDMD), GSDMB, GSDME.…”

Section: Mechanism Of Endothelial Injury By Homocysteinementioning

confidence: 99%

Mechanism of homocysteine-mediated endothelial injury and its consequences for atherosclerosis

Yuan

Chu

Lin

et al. 2023

Front. Cardiovasc. Med.

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Homocysteine (Hcy) is an intermediate amino acid formed during the conversion from methionine to cysteine. When the fasting plasma Hcy level is higher than 15 μmol/L, it is considered as hyperhomocysteinemia (HHcy). The vascular endothelium is an important barrier to vascular homeostasis, and its impairment is the initiation of atherosclerosis (AS). HHcy is an important risk factor for AS, which can promote the development of AS and the occurrence of cardiovascular events, and Hcy damage to the endothelium is considered to play a very important role. However, the mechanism by which Hcy damages the endothelium is still not fully understood. This review summarizes the mechanism of Hcy-induced endothelial injury and the treatment methods to alleviate the Hcy induced endothelial dysfunction, in order to provide new thoughts for the diagnosis and treatment of Hcy-induced endothelial injury and subsequent AS-related diseases.

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Section: Mechanism Of Endothelial Injury By Homocysteinementioning

confidence: 99%

Mechanism of homocysteine-mediated endothelial injury and its consequences for atherosclerosis

Yuan

Chu

Lin

et al. 2023

Front. Cardiovasc. Med.

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“…ATV therapy improves isoprenaline attack-induced cardiac function and remodeling by reducing ferroptosis [ 43 ]. ATV reverses barrier dysfunction, oxidative stress, and ferroptosis in human lung microvascular endothelial cells induced by cigarette smoke extract [ 44 ].Our in vivo and in vitro study proved that ATV inhibited ferroptosis in I/R rat myocardium through the SMAD7/hepcidin pathway, which provides new insights for the clinical application of ATV in I/R myocardium.…”

Section: Discussionmentioning

confidence: 99%

Atorvastatin Inhibits Ferroptosis of H9C2 Cells by regulatingSMAD7/Hepcidin Expression to Improve Ischemia-Reperfusion Injury

Peng

Liao

Zhou

et al. 2022

Cardiology Research and Practice

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Background. Ferroptosis plays a key role in cardiomyopathy. Atorvastatin (ATV) has a protective effect on ischemia-reperfusion (I/R) cardiomyopathy. The purpose of this study is to elucidate the mechanism of ATV in I/R injury. Methods. H9C2 cells and cardiomyopathy rats were induced by hypoxia/reoxygenation (H/R) and I/R to construct in vitro and in vivo models. Cell viability was determined by CCK8. Cardiac histopathology was observed by HE staining. Transmission electron microscope (TEM) was used to observe the mitochondrial morphology. The reactive oxygen species (ROS) content in cells was analyzed by the biochemical method. ELISA was conducted to calculate the concentrations of total iron/Fe2+ and hepcidin. The expression of ferroptosis and SMAD pathway-related genes were detected by qPCR. Western blot was performed to detect the expression levels of ferroptosis and SMAD pathway-related proteins. Results. In H9C2 cells, ATV reversed the decline in cell viability, mitochondrial shrinkage, and ROS elevation induced by erastin or H/R. The concentration of total iron and Fe2+ in H/R-induced H9C2 cells increased, and the protein expression of FPN1 decreased. After ATV treatment, the concentration of total iron and Fe2+ decreased, and the protein expression of FPN1 increased. The expression of the SMAD7 gene in H/R-induced H9C2 cells decreased, and the expression of the hepcidin gene increased, which were reversed by ATV. When SMAD7 was knocked down, ATV treatment failed to produce the above effect. ATV also improved ferroptosis in I/R rat myocardium through the SMAD7/hepcidin pathway. Conclusions. ATV reversed the decline in H9C2 cell viability, mitochondrial shrinkage, and ROS elevation, and improved the myocardium ferroptosis through the SMAD7/hepcidin pathway in I/R rat.

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“…7 The ferroptosis induced by cigarettes occurred in other types of cells, including corneal epithelial cells, semen, and vascular smooth muscle cells. [23][24][25][26] The underlying mechanism might be related to endoplasmic reticulum stress, mitochondrial dysfunction, ferritinophagy, decreased levels of glutathione. 7,9,25,27,28 We verified that CSE induced ferroptosis in HBEs accompanied by a lower level of GPx4 and a higher level of ferritin components (FTH and FTL), consistent with the recent studies.…”

Section: Discussionmentioning

confidence: 99%

Ferroptosis‐associated cholesterol metabolism regulated by p85α in human bronchial epithelial cells with smoking

Wang

2022

Clinical and Translational Dis

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Tongxinluo prevents chronic obstructive pulmonary disease complicated with atherosclerosis by inhibiting ferroptosis and protecting against pulmonary microvascular barrier dysfunction

Cited by 33 publications

References 65 publications

Mechanism of homocysteine-mediated endothelial injury and its consequences for atherosclerosis

Mechanism of homocysteine-mediated endothelial injury and its consequences for atherosclerosis

Atorvastatin Inhibits Ferroptosis of H9C2 Cells by regulatingSMAD7/Hepcidin Expression to Improve Ischemia-Reperfusion Injury

Ferroptosis‐associated cholesterol metabolism regulated by p85α in human bronchial epithelial cells with smoking

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