CRIF1 deficiency induced mitophagy via p66shc-regulated ROS in endothelial cells

Piao, Shuyu; Nagar, Harsha; Kim, Seonhee; Lee, Ikjun; Jeon, Byeong Hwa; Kim, Tae-Hee; Kim, Cuk-Seong

doi:10.1016/j.bbrc.2019.11.109

Cited by 9 publications

(6 citation statements)

References 31 publications

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“…A study by Luo et al 27 confirmed that dynamin-related protein-1 (DRP-1) enhanced the inhibition of lipopolysaccharide (LPS)-induced EC permeability through the upregulation of mitophagy (Figure 2). Piao et al 28 showed that mitochondrial dysfunction caused by CR6-interacting factor 1 (CRIF1) deficiency resulted in increased ROS, which led to increased expression of mitochondrial redox protein P66SHc and elevated levels of mitophagy-related markers LC3II, Parkin, and PINK1, initiating mitophagy in human ECs. Downregulation of P66SHc can restore mitophagic function by reducing ROS levels.…”

Section: Role Of Mitophagy In Endothelial Cellsmentioning

confidence: 99%

Dual Role of Mitophagy in Cardiovascular Diseases

Meng

Hou

et al. 2021

Journal of Cardiovascular Pharmacology

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Mitophagy is involved in the development of various cardiovascular diseases, such as atherosclerosis, heart failure, myocardial ischemia/reperfusion injury, and hypertension. Mitophagy is essential for maintaining intracellular homeostasis and physiological function in most cardiovascular origin cells, such as cardiomyocytes, endothelial cells, and vascular smooth muscle cells. Mitophagy is crucial to ensuring energy supply by selectively removing dysfunctional mitochondria, maintaining a balance in the number of mitochondria in cells, ensuring the integrity of mitochondrial structure and function, maintaining homeostasis, and promoting cell survival. Substantial research has indicated a "dual" effect of mitophagy on cardiac function, with inadequate and increased mitochondrial degradation both likely to influence the progression of cardiovascular disease. This review summarizes the main regulatory pathways of mitophagy and emphasizes that an appropriate amount of mitophagy can prevent endothelial cell injury, vascular smooth muscle cell proliferation, macrophage polarization, and cardiomyocyte apoptosis, avoiding further progression of cardiovascular diseases.

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Section: Role Of Mitophagy In Endothelial Cellsmentioning

confidence: 99%

Dual Role of Mitophagy in Cardiovascular Diseases

Meng

Hou

et al. 2021

Journal of Cardiovascular Pharmacology

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“…Mitochondrial damage promotes mitochondrial reactive oxygen species (mtROS) production and the release of immunogenic and apoptogenic factors [ 15 ]. Mitochondrial autophagy (mitophagy) is a selective mechanism for elimination of damaged mitochondria, reduces mtROS generation and excessive inflammation, and can promote cell survival [ [16] , [17] , [18] , [19] ]. Recent studies have demonstrated a negative regulatory role of Cav-1 in global cellular autophagy.…”

Section: Introductionmentioning

confidence: 99%

Caveolin-1 controls mitochondrial damage and ROS production by regulating fission - fusion dynamics and mitophagy

et al. 2022

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“…Decreased CRIF1 stimulates p66shc expression, and upregulated p66shc further activates the generation of reactive oxygen species (ROS). As a result, mitophagy and endothelial activation are induced by p66shc-mediated ROS in endothelial cells ( 84 , 85 ). However, the effect of mitophagy in vascular disorders is controversial and needs to be further studied.…”

Section: Crif1 In Mitochondria-related Diseasesmentioning

confidence: 99%

Multifunctions of CRIF1 in cancers and mitochondrial dysfunction

Jiang

Xiang²,

Lin³

et al. 2022

Front. Oncol.

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Sustaining proliferative signaling and enabling replicative immortality are two important hallmarks of cancer. The complex of cyclin-dependent kinase (CDK) and its cyclin plays a decisive role in the transformation of the cell cycle and is also critical in the initiation and progression of cancer. CRIF1, a multifunctional factor, plays a pivotal role in a series of cell biological progresses such as cell cycle, cell proliferation, and energy metabolism. CRIF1 is best known as a negative regulator of the cell cycle, on account of directly binding to Gadd45 family proteins or CDK2. In addition, CRIF1 acts as a regulator of several transcription factors such as Nur77 and STAT3 and partly determines the proliferation of cancer cells. Many studies showed that the expression of CRIF1 is significantly altered in cancers and potentially regarded as a tumor suppressor. This suggests that targeting CRIF1 would enhance the selectivity and sensitivity of cancer treatment. Moreover, CRIF1 might be an indispensable part of mitoribosome and is involved in the regulation of OXPHOS capacity. Further, CRIF1 is thought to be a novel target for the underlying mechanism of diseases with mitochondrial dysfunctions. In summary, this review would conclude the latest aspects of studies about CRIF1 in cancers and mitochondria-related diseases, shed new light on targeted therapy, and provide a more comprehensive holistic view.

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CRIF1 deficiency induced mitophagy via p66shc-regulated ROS in endothelial cells

Cited by 9 publications

References 31 publications

Dual Role of Mitophagy in Cardiovascular Diseases

Dual Role of Mitophagy in Cardiovascular Diseases

Caveolin-1 controls mitochondrial damage and ROS production by regulating fission - fusion dynamics and mitophagy

Multifunctions of CRIF1 in cancers and mitochondrial dysfunction

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