Unfolded protein response in cardiovascular disease

Kubra, Khadeja‐Tul; Akhter, Mohammad S.; Uddin, Mohammad A.; Barabutis, Nektarios

doi:10.1016/j.cellsig.2020.109699

Cited by 32 publications

(25 citation statements)

References 120 publications

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“…An increased production of reactive oxygen species may either promote lung pathologies or kill the cancer cells ( 64 ). Based on recent observations, we feel that the delineation of UPR signaling in the lungs may reveal new therapeutic possibilities toward lung disease and reveal new targets for lung disease, including ALI/ARDS ( 56 , 65 , 66 ). Experimental murine models of ALI/ARDS with endothelial specific mutations in control of the activation/deactivation of UPR branches shall be used to investigate the unexplored depths of the UPR universe and reveal potential therapies against respiratory dysfunctions.…”

Section: Discussionmentioning

confidence: 96%

Unfolded Protein Response in Lung Health and Disease

Barabutis

2020

Front. Med.

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The unfolded protein response (UPR) is a complex element, destined to protect the cells against a diverse variety of extracellular and intracellular challenges. UPR activation devises highly efficient responses to counteract cellular threats. If those activities fail, it will dictate cellular execution. The current work focuses on the role of UPR in pulmonary function, by immersing into the highly interrelated network that operates toward the endothelial barrier function. A highly sophisticated UPR manipulation shall reveal new therapeutic possibilities against inflammatory lung disease, such as acute lung injury and acute respiratory distress syndrome.

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Section: Discussionmentioning

confidence: 96%

Unfolded Protein Response in Lung Health and Disease

Barabutis

2020

Front. Med.

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“…Unfolded protein response (UPR) is a molecular machinery consisting of the activating transcription factor 6 (ATF6), the protein kinase RNA-like ER kinase (PERK), and the inositol-requiring enzyme-1α (IRE1α). It ensures proper protein folding and maturation [ 67 ]. Several studies have reported the involvement of UPR in lung health and disease [ 68 ].…”

Section: Human Pulmonary Vasculaturementioning

confidence: 99%

P53 in the impaired lungs

Uddin

Barabutis

2020

DNA Repair

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Our laboratory is focused on investigating the supportive role of P53 towards the maintenance of lung homeostasis. Acute lung injury, acute respiratory distress syndrome, chronic obstructive pulmonary disease, pulmonary fibrosis, bronchial asthma, pulmonary arterial hypertension, pneumonia and tuberculosis are respiratory pathologies, associated with dysfunctions of this endothelium defender (P53). Herein we review the evolving role of P53 towards the aforementioned inflammatory disorders, to potentially reveal new therapeutic possibilities in pulmonary disease.

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“…Interestingly, excessive induction of ER stress contributes to abnormal degradation of damaged proteins and activation of caspase-dependent cell apoptosis [13]. ER-related cell apoptosis is characterized by increased levels of CHOP and caspase-12 [14,15]. In addition, previous studies have reported a close relationship between endothelial dysfunction and ER stress [16].…”

Section: Introductionmentioning

confidence: 99%

Melatonin Attenuates ox‐LDL‐Induced Endothelial Dysfunction by Reducing ER Stress and Inhibiting JNK/Mff Signaling

Xie¹,

Zhong

Guo

et al. 2021

Oxidative Medicine and Cellular Longevity

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Endothelial dysfunction, which is characterized by damage to the endoplasmic reticulum (ER) and mitochondria, is involved in a variety of cardiovascular disorders. Here, we explored whether mitochondrial damage and ER stress are associated with endothelial dysfunction. We also examined whether and how melatonin protects against oxidized low-density lipoprotein- (ox-LDL-) induced damage in endothelial cells. We found that CHOP, GRP78, and PERK expressions, which are indicative of ER stress, increased significantly in response to ox-LDL treatment. ox-LDL also induced mitochondrial dysfunction as evidenced by decreased mitochondrial membrane potential, increased mitochondrial ROS levels, and downregulation of mitochondrial protective factors. In addition, ox-LDL inhibited antioxidative processes, as evidenced by decreased antioxidative enzyme activity and reduced Nrf2/HO-1 expression. Melatonin clearly reduced ER stress and promoted mitochondrial function and antioxidative processes in the presence of ox-LDL. Molecular investigation revealed that ox-LDL activated the JNK/Mff signaling pathway, and melatonin blocked this effect. These results demonstrate that ox-LDL induces ER stress and mitochondrial dysfunction and activates the JNK/Mff signaling pathway, thereby contributing to endothelial dysfunction. Moreover, melatonin inhibited JNK/Mff signaling and sustained ER homeostasis and mitochondrial function, thereby protecting endothelial cells against ox-LDL-induced damage.

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Unfolded protein response in cardiovascular disease

Cited by 32 publications

References 120 publications

Unfolded Protein Response in Lung Health and Disease

Unfolded Protein Response in Lung Health and Disease

P53 in the impaired lungs

Melatonin Attenuates ox‐LDL‐Induced Endothelial Dysfunction by Reducing ER Stress and Inhibiting JNK/Mff Signaling

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