Roles and Therapeutic Implications of Endoplasmic Reticulum Stress and Oxidative Stress in Cardiovascular Diseases

Zhou, Yan; Murugan, Dharmani Devi; Khan, Haroon; Huang, Yü; Cheang, Wai San

doi:10.3390/antiox10081167

Cited by 49 publications

(46 citation statements)

References 175 publications

(185 reference statements)

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“…As the main innate immune cells, macrophages play a key role in maintaining the inflammatory response of blood vessels and regulating the stability of atherosclerotic plaques by producing pro-inflammatory cytokines ( Kim et al, 2021 ). Moreover, macrophages promote the development of atherosclerosis in other ways, such as through endoplasmic reticulum (ER) stress and autophagy ( Zhou et al, 2021 ). Although the exact mechanism behind macrophage regulation of atherosclerosis is unclear, certain kinases seem to hold the key to determine macrophage phenotype and function.…”

Section: Introductionmentioning

confidence: 99%

LKB1 Regulates Vascular Macrophage Functions in Atherosclerosis

et al. 2021

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Liver kinase B1 (LKB1) is known to shape the regulation of macrophage function by participating in multiple processes including cell metabolism, growth, and polarization. However, whether LKB1 also affects the functional plasticity of macrophages in atherosclerosis has not attracted much attention. Abnormal macrophage function is a pathophysiological hallmark of atherosclerosis, characterized by the formation of foam cells and the maintenance of vascular inflammation. Mounting evidence supports that LKB1 plays a vital role in the regulation of macrophage function in atherosclerosis, including affecting lipid metabolism reprogramming, inflammation, endoplasmic reticulum stress, and autophagy in macrophages. Thus, decreased expression of LKB1 in atherosclerosis aggravates vascular injury by inducing excessive lipid deposition in macrophages and the formation of foam cells. To systematically understand the role and potential mechanism of LKB1 in regulating macrophage functions in atherosclerosis, this review summarizes the relevant data in this regard, hoping to provide new ideas for the prevention and treatment of atherosclerosis.

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Section: Introductionmentioning

confidence: 99%

LKB1 Regulates Vascular Macrophage Functions in Atherosclerosis

et al. 2021

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“…The subunit of G βγ also regulates adenylyl cyclase, phospholipase C- β (PLC- β ), phospholipase A2 (PLA2), phosphoinositide 3-kinase (PI3-kinase), and β -adrenergic receptor kinase, some of which induce calcium regulation [ 6 , 21 , 22 ]. Increased levels of calcium always trigger the production of ROS [ 23 ], and excessive ROS subsequently resulted in damage of NPCs or IVDs [ 17 ], which was thought to be one of the mechanisms of GPR35-induced IDD.…”

Section: Discussionmentioning

confidence: 99%

G-Protein Coupled Receptor 35 Induces Intervertebral Disc Degeneration by Mediating the Influx of Calcium Ions and Upregulating Reactive Oxygen Species

Chen

Jiao

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Intervertebral disc degeneration (IDD) is a chronic disease affecting millions of patients; however, its specific etiology is unknown. G protein-coupled receptors (GPRs) are a superfamily of integral membrane receptors in cells, and the receptors respond to a diverse range of stimuli and participate in multiple cellular activities. Here, using RNA-sequencing (RNA-seq) methods and immunohistochemistry, we revealed that G protein-coupled receptor 35 (GPR35) may have a relationship with IDD. Then, we demonstrated that the deletion of GPR35 in nucleus pulposus cells (NPCs) with siRNA or in Gpr35-/- mice significantly alleviated IDD caused by senescence or mechanical stress, further validating the pathological role of GPR35 in IDD. In addition, GPR35 induced the influx of Ca2+ and upregulation of reactive oxygen species (ROS) under mechanical stress in NPCs, which we believe to be the mechanism of GPR35-induced IDD. Finally, GPR35 caused upregulation of ROS in NPCs under mechanical stress, while excessive ROS stimulated the NPCs to express more GPR35 with a significant dose or time response. The u-regulated GPR35 could sense mechanical stress to produce more ROS and perpetuate this harmful cycle. In summary, our study shows that GPR35 plays a critical role in mediating IDD via mediating the influx of calcium ions and upregulating ROS, which implies a strong potential advantage of GPR35 as a prevention and treatment target in IDD.

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“…Oxidative stress is defined as an imbalance between the generation of reactive oxygen species (ROS) and the endogenous antioxidant defense mechanisms ( Zhou Y et al, 2021 ). At low concentrations, ROS modulates critical functions in cell homeostasis, whereas an overabundance of ROS plays a crucial role of worsening of the systolic and diastolic function and HF ( Munzel et al, 2015 ).…”

Section: Mechanisms Of Traditional Chinese Medicine In Treating Heart...mentioning

confidence: 99%

Mechanisms and Efficacy of Traditional Chinese Medicine in Heart Failure

et al. 2022

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Heart failure (HF) is one of the main public health problems at present. Although some breakthroughs have been made in the treatment of HF, the mortality rate remains very high. However, we should also pay attention to improving the quality of life of patients with HF. Traditional Chinese medicine (TCM) has a long history of being used to treat HF. To demonstrate the clinical effects and mechanisms of TCM, we searched published clinical trial studies and basic studies. The search results showed that adjuvant therapy with TCM might benefit patients with HF, and its mechanism may be related to microvascular circulation, myocardial energy metabolism, oxidative stress, and inflammation.

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Roles and Therapeutic Implications of Endoplasmic Reticulum Stress and Oxidative Stress in Cardiovascular Diseases

Cited by 49 publications

References 175 publications

LKB1 Regulates Vascular Macrophage Functions in Atherosclerosis

LKB1 Regulates Vascular Macrophage Functions in Atherosclerosis

G-Protein Coupled Receptor 35 Induces Intervertebral Disc Degeneration by Mediating the Influx of Calcium Ions and Upregulating Reactive Oxygen Species

Mechanisms and Efficacy of Traditional Chinese Medicine in Heart Failure

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