Endoplasmic reticulum stress and focused drug discovery in cardiovascular disease

Yang, Yiyuan; Zhou, Qi; Gao, Anbo; Chen, Linxi; Li, Lanfang

doi:10.1016/j.cca.2020.01.031

Cited by 32 publications

(21 citation statements)

References 110 publications

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“…Different pathologies, such as diabetes mellitus [ 340 ], obesity [ 341 , 342 ], cardiovascular disease [ 343 , 344 ] and CKD [ 345 , 346 ], have been associated with ER stress. In CRS, the activation of ER stress in the heart and kidney could be induced by different factors, such as hemodynamic changes, hormones from the RAAS, inflammation or oxidative stress [ 346 , 347 , 348 ].…”

Section: Mechanisms Involved In Fibrosis Progressionmentioning

confidence: 99%

Fibrosis, the Bad Actor in Cardiorenal Syndromes: Mechanisms Involved

Delgado-Valero

Cachofeiro

Martínez‐Martínez

2021

Cells

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Cardiorenal syndrome is a term that defines the complex bidirectional nature of the interaction between cardiac and renal disease. It is well established that patients with kidney disease have higher incidence of cardiovascular comorbidities and that renal dysfunction is a significant threat to the prognosis of patients with cardiac disease. Fibrosis is a common characteristic of organ injury progression that has been proposed not only as a marker but also as an important driver of the pathophysiology of cardiorenal syndromes. Due to the relevance of fibrosis, its study might give insight into the mechanisms and targets that could potentially be modulated to prevent fibrosis development. The aim of this review was to summarize some of the pathophysiological pathways involved in the fibrotic damage seen in cardiorenal syndromes, such as inflammation, oxidative stress and endoplasmic reticulum stress, which are known to be triggers and mediators of fibrosis.

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Section: Mechanisms Involved In Fibrosis Progressionmentioning

confidence: 99%

Fibrosis, the Bad Actor in Cardiorenal Syndromes: Mechanisms Involved

Delgado-Valero

Cachofeiro

Martínez‐Martínez

2021

Cells

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“…Of note, low molecular weight chemical chaperones, PBA and TUDCA, which are both approved by the US Food and Drug Administration (FDA), were shown to improve protein folding and reduce ER stress response both in cultured cells and in in vivo studies. These compounds were reported to improve glucose response and insulin signaling, endothelial cell dysfunction, hypertrophy, fibrosis and atherosclerosis [ 48 , 49 ].…”

Section: Er Stress and Endothelial Dysfunctionmentioning

confidence: 99%

“…Multiple regulators and modulators for the various arms of the UPR were reported in the literature [ 48 , 49 ]. Several agents were found to enhance the expression levels of BiP in animal models.…”

Section: Er Stress and Endothelial Dysfunctionmentioning

confidence: 99%

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Interplay between Endoplasmic Reticulum Stress and Large Extracellular Vesicles (Microparticles) in Endothelial Cell Dysfunction

et al. 2020

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Upon increased demand for protein synthesis, accumulation of misfolded and/or unfolded proteins within the endoplasmic reticulum (ER), a pro-survival response is activated termed unfolded protein response (UPR), aiming at restoring the proper function of the ER. Prolonged activation of the UPR leads, however, to ER stress, a cellular state that contributes to the pathogenesis of various chronic diseases including obesity and diabetes. ER stress response by itself can result in endothelial dysfunction, a hallmark of cardiovascular disease, through various cellular mechanisms including apoptosis, insulin resistance, inflammation and oxidative stress. Extracellular vesicles (EVs), particularly large EVs (lEVs) commonly referred to as microparticles (MPs), are membrane vesicles. They are considered as a fingerprint of their originating cells, carrying a variety of molecular components of their parent cells. lEVs are emerging as major contributors to endothelial cell dysfunction in various metabolic disease conditions. However, the mechanisms underpinning the role of lEVs in endothelial dysfunction are not fully elucidated. Recently, ER stress emerged as a bridging molecular link between lEVs and endothelial cell dysfunction. Therefore, in the current review, we summarized the roles of lEVs and ER stress in endothelial dysfunction and discussed the molecular crosstalk and relationship between ER stress and lEVs in endothelial dysfunction.

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“…The endoplasmic reticulum (ER) is involved in protein synthesis, post-translational modifications, and correct folding of proteins, and plays a key role in many cellular processes. 1,2 The endoplasmic reticulum is highly sensitive to changes in a range of intracellular environment or extracellular stimuli, especially in malignant cells, including hypoxia, increased protein synthesis, impaired ubiquitination and proteasomal degradation, insufficient energy, nutrition, excessive or restricted substances, and imbalanced calcium levels. [3][4][5] These stimuli can lead to accumulation of misfolded proteins in the endoplasmic reticulum cavity, and when the accumulation of misfolded proteins in the endoplasmic reticulum exceeds a certain level, the endoplasmic reticulum will initiate a series of unfolded protein reactions (UPR) to ensure a balance between protein folding capacity and demand.…”

Section: Introductionmentioning

confidence: 99%

Biological Function of HYOU1 in Tumors and Other Diseases

Rao¹,

Oyang²,

Liang³

et al. 2021

OTT

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Various stimuli induce an unfolded protein response to endoplasmic reticulum stress, accompanied by the expression of endoplasmic reticulum molecular chaperones. Hypoxia-upregulated 1 gene (HYOU1) is a chaperone protein located in the endoplasmic reticulum. HYOU1 expression was upregulated in many diseases, including various cancers and endoplasmic reticulum stress-related diseases. HYOU1 does not only play an important protective role in the occurrence and development of tumors, but also is a potential therapeutic target for cancer. HYOU1 may also be used as an immune stimulation adjuvant because of its anti-tumor immune response, and a molecular target for therapy of many endoplasmic reticulum-related diseases. In this article, we summarize the updates in HYOU1 and discuss the potential therapeutic effects of HYOU1.

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Endoplasmic reticulum stress and focused drug discovery in cardiovascular disease

Cited by 32 publications

References 110 publications

Fibrosis, the Bad Actor in Cardiorenal Syndromes: Mechanisms Involved

Fibrosis, the Bad Actor in Cardiorenal Syndromes: Mechanisms Involved

Interplay between Endoplasmic Reticulum Stress and Large Extracellular Vesicles (Microparticles) in Endothelial Cell Dysfunction

Biological Function of HYOU1 in Tumors and Other Diseases

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