Endoplasmic reticulum stress at the crossroads of progeria and atherosclerosis

Pasquale, Elisa Di; Condorelli, Gianluigi

doi:10.15252/emmm.201910360

Cited by 11 publications

(6 citation statements)

References 12 publications

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“…A great deal of research indicates that ER stress occurs in a variety of cell types involved in AS including endothelial cells and macrophages and also influences the disease process of AS by coordinating protein and lipid metabolism, inflammatory response, various stress responses, and cell death [13, 72–78]. Similarly, the NLRP3 inflammasome and its genetic variants are involved in atherosclerotic pathogenesis [79, 80].…”

Section: The Molecular Pathways Between Er Stress and Nlrp3 Inflammentioning

confidence: 99%

ER Stress Activates the NLRP3 Inflammasome: A Novel Mechanism of Atherosclerosis

Chen

Guo

et al. 2019

Oxidative Medicine and Cellular Longevity

100

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The endoplasmic reticulum (ER) is an important organelle that regulates several fundamental cellular processes, and ER dysfunction has implications for many intracellular events. The nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome is an intracellularly produced macromolecular complex that can trigger pyroptosis and inflammation, and its activation is induced by a variety of signals. ER stress has been found to affect NLRP3 inflammasome activation through multiple effects including the unfolded protein response (UPR), calcium or lipid metabolism, and reactive oxygen species (ROS) generation. Intriguingly, the role of ER stress in inflammasome activation has not attracted a great deal of attention. In addition, increasing evidence highlights that both ER stress and NLRP3 inflammasome activation contribute to atherosclerosis (AS). AS is a common cardiovascular disease with complex pathogenesis, and the precise mechanisms behind its pathogenesis remain to be determined. Both ER stress and the NLRP3 inflammasome have emerged as critical individual contributors of AS, and owing to the multiple associations between these two events, we speculate that they contribute to the mechanisms of pathogenesis in AS. In this review, we aim to summarize the molecular mechanisms of ER stress, NLRP3 inflammasome activation, and the cross talk between these two pathways in AS in the hopes of providing new pharmacological targets for AS treatment.

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Section: The Molecular Pathways Between Er Stress and Nlrp3 Inflammentioning

confidence: 99%

ER Stress Activates the NLRP3 Inflammasome: A Novel Mechanism of Atherosclerosis

Chen

Guo

et al. 2019

Oxidative Medicine and Cellular Longevity

100

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“…ER stress, oxidative stress, and inflammatory response together make up defense networks of the cells that react to outside stimuli [ 8 , 61 ]. Risk factors related to AS, such as hyperlipidemia, hypertension, and obesity, activated the ER stress-related proteins, such as IRE1, PERK, and ATF6, and aggravated the inflammatory response in macrophages [ 62 , 63 ]. UPR activation and ER stress had been identified in atherosclerotic lesions.…”

Section: Discussionmentioning

confidence: 99%

BTK Promotes Atherosclerosis by Regulating Oxidative Stress, Mitochondrial Injury, and ER Stress of Macrophages

Qiu

Chen

et al. 2021

Oxidative Medicine and Cellular Longevity

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Atherosclerosis (AS) is a chronic metabolic disease in arterial walls, characterized by lipid deposition and persistent aseptic inflammation. AS is regarded as the basis of a variety of cardiovascular and cerebrovascular diseases. It is widely acknowledged that macrophages would become foam cells after internalizing lipoprotein particles, which is an initial factor in atherogenesis. Here, we showed the influences of Bruton’s tyrosine kinase (BTK) in macrophage-mediated AS and how BTK regulates the inflammatory responses of macrophages in AS. Our bioinformatic results suggested that BTK was a potential hub gene, which is closely related to oxidative stress, ER stress, and inflammation in macrophage-induced AS. Moreover, we found that BTK knockdown could restrain ox-LDL-induced NK-κB signaling activation in macrophages and repressed M1 polarization. The mechanistic studies revealed that oxidative stress, mitochondrial injury, and ER stress in macrophages were also suppressed by BTK knockdown. Furthermore, we found that sh-BTK adenovirus injection could alleviate the severity of AS in ApoE-/- mice induced by a high-fat diet in vivo. Our study suggested that BTK promoted ox-LDL-induced ER stress, oxidative stress, and inflammatory responses in macrophages, and it may be a potential therapeutic target in AS.

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“…A number of scientists have identified a relationship between endoplasmic reticulum stress and the occurrence of atherosclerosis [ 222 , 223 , 224 , 225 , 226 , 227 ]. It was found that ER stress occurs in cells involved in the occurrence and development of atherosclerosis, including endothelial cells and macrophages.…”

Section: The Relationship Of Chronic Stress With the Occurrence Anmentioning

confidence: 99%

Some Molecular and Cellular Stress Mechanisms Associated with Neurodegenerative Diseases and Atherosclerosis

Sinyov

Рыжкова

Sazonova

et al. 2021

IJMS

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Chronic stress is a combination of nonspecific adaptive reactions of the body to the influence of various adverse stress factors which disrupt its homeostasis, and it is also a corresponding state of the organism’s nervous system (or the body in general). We hypothesized that chronic stress may be one of the causes occurence of several molecular and cellular types of stress. We analyzed literary sources and considered most of these types of stress in our review article. We examined genes and mutations of nuclear and mitochondrial genomes and also molecular variants which lead to various types of stress. The end result of chronic stress can be metabolic disturbance in humans and animals, leading to accumulation of reactive oxygen species (ROS), oxidative stress, energy deficiency in cells (due to a decrease in ATP synthesis) and mitochondrial dysfunction. These changes can last for the lifetime and lead to severe pathologies, including neurodegenerative diseases and atherosclerosis. The analysis of literature allowed us to conclude that under the influence of chronic stress, metabolism in the human body can be disrupted, mutations of the mitochondrial and nuclear genome and dysfunction of cells and their compartments can occur. As a result of these processes, oxidative, genotoxic, and cellular stress can occur. Therefore, chronic stress can be one of the causes forthe occurrence and development of neurodegenerative diseases and atherosclerosis. In particular, chronic stress can play a large role in the occurrence and development of oxidative, genotoxic, and cellular types of stress.

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Endoplasmic reticulum stress at the crossroads of progeria and atherosclerosis

Cited by 11 publications

References 12 publications

ER Stress Activates the NLRP3 Inflammasome: A Novel Mechanism of Atherosclerosis

ER Stress Activates the NLRP3 Inflammasome: A Novel Mechanism of Atherosclerosis

BTK Promotes Atherosclerosis by Regulating Oxidative Stress, Mitochondrial Injury, and ER Stress of Macrophages

Some Molecular and Cellular Stress Mechanisms Associated with Neurodegenerative Diseases and Atherosclerosis

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