Estrogen prevent atherosclerosis by attenuating endothelial cell pyroptosis via activation of estrogen receptor α-mediated autophagy

Meng, Qingcai; Yu, Li; Ji, Tingting; Cao, Ying; Li, Jun; Fu, Yu; Wang, Suyun; Chen, Qi; Chen, Wen; Huang, Fuhua; Wang, Youran; Zhang, Qichun; Wang, Xiaoliang; Bian, Huimin

doi:10.1016/j.jare.2020.08.010

Cited by 111 publications

(84 citation statements)

References 57 publications

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“…The reaction can ameliorate atherosclerosis as early as possible, usually before the menopausal stage. 224 Trimethylamine N‐oxide (TMAO) is usually generated from the phosphatidylcholine metabolism of gut flora, which also presents as a danger signal for cardiovascular diseases. TMAO promotes ROS‐induced pyroptosis in vascular ECs through the upregulation of the succinate dehydrogenase complex subunit B (SDHB), thereby contributing to the progression of atherosclerotic lesions.…”

Section: The Relationship Between Pyroptosis and Metabolismmentioning

confidence: 99%

“…As for estrogen, it inhibits pyroptosis in vascular ECs mainly through the estrogen receptor alpha (ER‐α)‐mediated activation of autophagy. The reaction can ameliorate atherosclerosis as early as possible, usually before the menopausal stage 224 . Trimethylamine N‐oxide (TMAO) is usually generated from the phosphatidylcholine metabolism of gut flora, which also presents as a danger signal for cardiovascular diseases.…”

Section: The Relationship Between Pyroptosis and Metabolismmentioning

confidence: 99%

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Pyroptosis, metabolism, and tumor immune microenvironment

Gao

et al. 2021

Clinical & Translational Med

178

121

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In response to a wide range of stimulations, host cells activate pyroptosis, a kind of inflammatory cell death which is provoked by the cytosolic sensing of danger signals and pathogen infection. In manipulating the cleavage of gasdermins (GSDMs), researchers have found that GSDM proteins serve as the real executors and the deterministic players in fate decisions of pyroptotic cells. Whether inflammatory characteristics induced by pyroptosis could cause damage the host or improve immune activity is largely dependent on the context, timing, and response degree. Here, we systematically review current points involved in regulatory mechanisms and the multidimensional roles of pyroptosis in several metabolic diseases and the tumor microenvironment. Targeting pyroptosis may reveal potential therapeutic avenues.

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Section: The Relationship Between Pyroptosis and Metabolismmentioning

confidence: 99%

Section: The Relationship Between Pyroptosis and Metabolismmentioning

confidence: 99%

Pyroptosis, metabolism, and tumor immune microenvironment

Gao

et al. 2021

Clinical & Translational Med

178

121

View full text Add to dashboard Cite

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“…On the other hand, existing studies have indicated that multiple drugs and genes such as melatonin, salidroside (SAL), estrogen, pyrogallol-phloroglucinol-6,6-bieckol (PPB) and fibroblast growth factor 21 (FGF21) decrease atherosclerosis plaque formation via inhibiting ECs pyroptosis in vivo and in vitro ( Zhang et al, 2018 ; Oh et al, 2020 ; Xing et al, 2020 ; Zeng et al, 2020 ; Meng et al, 2021 ). Moreover, recent studis have discovered more drugs and miRNAs that could regulate ECs pyroptosis, including atorvastatin, miRNA-30c-5p, miRNA-125a-5p, etc.…”

Section: Pyroptosis In Atherosclerosismentioning

confidence: 99%

“…A recent study showed that estrogen inhibits ECs pyroptosis by inducing autophagy, thereby ameliorating atherosclerosis in mice. Estrogen reduced the expression of caspase-1 and GSDMD in homocysteine (Hcy)-treated HUVECs, while the autophagy inhibitor 3-MA reversed this effect ( Meng et al, 2021 ). Meanwhile, Jiang et al reported that autophagy alleviates the activation of NLRP3 inflammasome and pyroptosis caused by acrolein in ECs via improving mitochondrial function and reducing ROS ( Jiang et al, 2018 ).…”

Section: Pyroptosis In Atherosclerosismentioning

confidence: 99%

Pyroptosis in the Initiation and Progression of Atherosclerosis

Qian

Zhao²,

Wan³

et al. 2021

Front. Pharmacol.

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Pyroptosis, a newly discovered form of programmed cell death, is characterized by cell swelling, the protrusion of large bubbles from the plasma membrane and cell lysis. This death pathway is mediated by the pore formation of gasdermin D (GSDMD), which is activated by human caspase-1/caspase-4/caspase-5 (or mouse caspase-1/caspase11), and followed with the releasing of both cell contents and proinflammatory cytokines. Pyroptosis was initially found to function as an innate immune effector mechanism to facilitate host defense against pathogenic microorganisms, and subsequent studies revealed that pyroptosis also plays an eventful role in inflammatory immune diseases and tumor resistance. Recent studies have also shown that pyroptosis is involved in the initiation, the progression and complications of atherosclerosis. Here, we provide an overview of the role of pyroptosis in atherosclerosis by focusing on three important participating cells: ECs, macrophages, and SMCs. In addition, we also summarized drugs and stimuli that regulate the progression of atherosclerosis by influencing cell pyroptosis.

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“…Torii et al found that the lysosomal inhibitor Baf-A1 reduces ferroptosis of tumor cells ( 20 ). It has been previously suggested that the autophagy-lysosome pathway inhibits CVD progression ( 21 , 22 ). However, most of the current studies on the relationship between the autophagy-lysosome pathway and ferroptosis have focused on tumor cells with the findings suggesting that autophagy promotes ferroptosis.…”

Section: Role Of Organelles In the Regulation Of Ferroptosismentioning

confidence: 99%

The Role of Ferroptosis in Cardiovascular Disease and Its Therapeutic Significance

Chen

Yan

et al. 2021

Front. Cardiovasc. Med.

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Cardiovascular diseases (CVDs) are the leading cause of deaths worldwide with regulated cell death playing an important role in cardiac pathophysiology. However, the classical mode of cell death cannot fully explain the occurrence and development of heart disease. In recent years, much research has been performed on ferroptosis, a new type of cell death that causes cell damage and contributes to the development of atherosclerosis, myocardial infarction, heart failure, and other diseases. In this review, we discuss the role of different organelles in ferroptosis and also focus on the relationship between autophagy and ferroptosis. Additionally, we describe the specific mechanism by which ferroptosis contributes to the development of CVD. Finally, we summarize the current research on ferroptosis-related pathway inhibitors and the applications of clinically beneficial cardiovascular drugs.

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Estrogen prevent atherosclerosis by attenuating endothelial cell pyroptosis via activation of estrogen receptor α-mediated autophagy

Abstract: Graphical abstract

Cited by 111 publications

References 57 publications

Pyroptosis, metabolism, and tumor immune microenvironment

Pyroptosis, metabolism, and tumor immune microenvironment

Pyroptosis in the Initiation and Progression of Atherosclerosis

The Role of Ferroptosis in Cardiovascular Disease and Its Therapeutic Significance

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