Regulation of efferocytosis by caspase-dependent apoptotic cell death in atherosclerosis

Tajbakhsh, Amir; Kovanen, Petri T.; Rezaee, Mehdi; Banach, Maciej; Moallem, Seyed Adel; Sahebkar, Amirhossein

doi:10.1016/j.biocel.2020.105684

Cited by 28 publications

(16 citation statements)

References 125 publications

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“…This is explained by the fact that the role of the ATP-dependent ATP enzyme ATP11 restricts PtdSer to the inner leaflet of the plasma membrane under normal circumstances. In the process of apoptosis, caspase3 cleavage inactivates ATP11 and promotes the exposure of PtdSer on the surface of ACs ( 34 ). Thus, the lack of such signals could lead to the accumulation of ACs and drive the occurrence of AS.…”

Section: Basic Efferocytosis Proceduresmentioning

confidence: 99%

Potential Mechanisms and Effects of Efferocytosis in Atherosclerosis

Wang

Tang

et al. 2021

Front. Endocrinol.

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Atherosclerosis (AS) is the main pathological basis for the development of cardio-cerebrovascular diseases. Abnormal accumulation of apoptotic and necrotic cells resulted in plaque enlargement, necrotic core formation and plaque rupture in AS. Under physiological conditions, apoptotic cells (ACs) could be effectively phagocytized and cleared by phagocyte-mediated efferocytosis. In contrast, the clearance efficiency of ACs in AS plaque was much lower because of the impaired efferocytosis in AS. Recent findings have made great progress on the molecular mechanisms of efferocytosis process and dynamic regulation, and its dysfunction on organismal health. Yet, there are still few effective treatments for this process. This article reviews the mechanism of efferocytosis and the role of efferocytosis in AS, highlighting a novel therapeutic strategy for AS, which mainly prevents the progression of plaque by targeting efferocytosis.

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Section: Basic Efferocytosis Proceduresmentioning

confidence: 99%

Potential Mechanisms and Effects of Efferocytosis in Atherosclerosis

Wang

Tang

et al. 2021

Front. Endocrinol.

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“…at is to say, the progressive deposition of lipids in the artery walls which causes the artery walls to thicken and harden [44]. In this case, one speaks more often of atherosclerosis in reference to atheroma, which refers to the plaque of fat formed.…”

Section: Study Of the Influence Of The Elasticity Modulus (Ep)mentioning

confidence: 99%

Study of the Influence of Plaque Growth and Hydrostatic Properties in an Atherosclerotic Artery, for the Prevention of Arterial Wall Damage: Application to Vascular Diseases

Nzifack

Takam

Toussaint

et al. 2021

Advances in Materials Science and Engineering

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The objective of this work is to prevent damage of the arterial wall, using a theoretical model of hyperelastic, anisotropic, and dynamic behavior of the human arterial. This work is mainly focused on the properties of the hydrostatic stress and the evolution of stenosis. This work is mainly focused on the properties of the hydrostatic stress and the evolution of stenosis in order to understand the effect of the size of the plaque deposit, the loss of elasticity of the wall, and the increase in the density of the blood on the mechanical behavior of the human arterial wall. The great contribution of this work shows us that increasing the size of the plaque also increases arterial stress, and the radial growth of the plaque is very dangerous compared to the longitudinal growth. Furthermore, atherosclerosis promotes the loss of elasticity of the arterial wall and increases the density of blood mass. Indeed, all these subsequent phenomena increase arterial stress. All the results are in good agreement with the expected result of the literature and could play an important role in the diagnosis of the patient with an arterial injury. It will also help the doctor and the surgeon to make a good clinical decision and good treatment planning.

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“…Previous studies have shown that there are excessive numbers of apoptotic macrophages in vulnerable plaques (22). Abundant evidence also confirms that macrophage apoptosis directly causes plaque instability and increases the risk of adverse cardiovascular events (23)(24)(25). Therefore, a search for the underlying upstream target that regulates macrophage apoptosis has important clinical implications for assessing the risk of vulnerable plaque formation in patients with atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

“…Excessive numbers of apoptotic macrophages are found in vulnerable plaques (22). Macrophage apoptosis causes plaque instability and increases risk of adverse cardiovascular events (23–25). Knowledge of upstream targets that regulate macrophage apoptosis would aid clinical assessment of the risk of vulnerable plaque formation.…”

Section: Introductionmentioning

confidence: 99%

IRGM/Irgm1 Aggravates Progression of Atherosclerosis by Inducing Macrophage Apoptosis through the MAPK Signaling Pathway

Fang

Sun

Cai

et al. 2021

Preprint

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Acute coronary syndrome (ACS) caused by plaque rupture (PR) is the chief culprit behind cardiovascular death, yet its exact mechanism remains unclear. Immunity-related GTPase (IRGM/Irgm1) has been widely studied in several inflammatory diseases, but the role of IRGM/Irgm1 in atherosclerosis is poorly characterized. Here, we shed light on the mechanism by which IRGM/Irgm1 contributes to plaque vulnerability in atherosclerosis. We first identified ruptured and non-ruptured plaques by optical coherence tomography, and strikingly found that serum IRGM was highly expressed in ST-segment elevation myocardial infarction patients with PR. Next, we used ApoE-/-Irgm1+/+ and ApoE-/-Irgm1+/- mice and corresponding bone marrow chimeras to establish a model for advanced atherosclerosis, and found that Irgm1 could aggravate progression of atherosclerotic plaques. We confirmed that Irgm1 contributes to macrophage apoptosis by promoting the production of reactive oxygen species. Finally, we discovered that Irgm1 induces macrophage apoptosis by activating the MAPK signaling pathway. Our findings highlight the mechanism by which IRGM/Irgm1 contributes to the formation of vulnerable plaques and may offer a novel target for the timely treatment of ACS.

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Regulation of efferocytosis by caspase-dependent apoptotic cell death in atherosclerosis

Cited by 28 publications

References 125 publications

Potential Mechanisms and Effects of Efferocytosis in Atherosclerosis

Potential Mechanisms and Effects of Efferocytosis in Atherosclerosis

Study of the Influence of Plaque Growth and Hydrostatic Properties in an Atherosclerotic Artery, for the Prevention of Arterial Wall Damage: Application to Vascular Diseases

IRGM/Irgm1 Aggravates Progression of Atherosclerosis by Inducing Macrophage Apoptosis through the MAPK Signaling Pathway

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