Mitochondrial Quality Control as a Therapeutic Target

Suliman, Hagir B.; Piantadosi, Claude A.

doi:10.1124/pr.115.011502

Cited by 231 publications

(175 citation statements)

References 366 publications

(380 reference statements)

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“…proteins participate in maintaining mitochondrial quality control via their effects on mitochondrial protein import, fission/fusion, and macro-autophagy. 57 An increasing number of select BCL-2 proteins regulate normal cell metabolism. 4 Specific BCL-2 proteins regulate carbon substrate use by activating a "fuel switch" that determines which intracellular substrate is favored.…”

Section: Bcl-2 Proteins and Mitochondrial Function: Morphogenesis Dymentioning

confidence: 99%

The Role of BCL-2 Family Members in Acute Kidney Injury

Borkan

2016

Seminars in Nephrology

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Section: Bcl-2 Proteins and Mitochondrial Function: Morphogenesis Dymentioning

confidence: 99%

The Role of BCL-2 Family Members in Acute Kidney Injury

Borkan

2016

Seminars in Nephrology

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“…The estrogen receptor-β (ERβ) localizes to the mitochondria in a ligand-dependent or ligand-independent manner. A reduction in mitochondrial function via decreasing circulating estrogen is the standard treatment for endometriosis [5]. These data indicate that mitochondria homeostasis could be considered a therapeutic target for the treatment of endometriosis.…”

Section: Introductionmentioning

confidence: 97%

Effect of Mst1 on Endometriosis Apoptosis and Migration: Role of Drp1-Related Mitochondrial Fission and Parkin-Required Mitophagy

Zhao

Yang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Mitochondrial homeostasis is implicated in the development and progression of endometriosis through poorly defined mechanisms. Mst1 is the major growth suppressor related to cancer migration, apoptosis and proliferation. However, whether Mst1 is involved in endometriosis apoptosis and migration via regulating the mitochondrial function remains to be elucidated. Methods: Expression of Mst1 in endometriosis was examined via western blots. Cellular apoptosis was detected via MTT and TUNEL assay. Gain of function assay about Mst1 was conducted via adenovirus over-expression. Mitochondrial functions were evaluated via mitochondrial membrane potential JC-1 staining, ROS flow cytometry analysis, mPTP opening assessment and immunofluorescence of HtrA2/Omi. The mitophagy activity were examined via western blots and immunofluorescence. Results: First, we found that Mst1 was significantly downregulated in the ectopic endometrium of endometriosis compared to the normal endometrium. However, the recovery of Mst1 function was closely associated with the inability of endometrial stromal cells (ESCs) to migrate and survive. A functional study indicated that regaining Mst1 enhanced Drp1 post-transcriptional phosphorylation at Ser616 and repressed Parkin transcription activity via p53, leading to mitochondrial fission activation and mitophagy inhibition. Excessive Drp1-related fission forced the mitochondria to liberate HtrA2/Omi into the cytoplasm. Moreover, Mst1-induced defective mitophagy evoked cellular

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“…An emerging and promising approach to treating these diseases leverages their sensitivity to activation of the master regulator of antioxidant and cytoprotective genes and their products, namely, nuclear factor (erythroid-derived 2)-like 2/antioxidant response element (Nrf2/ARE), and mitophagy [Osborne et al, 2014;Pagano et al, 2014;Palikaras and Tavernarakis, 2014;Johnson and Johnson, 2015;Joshi et al, 2015;Matic et al, 2015;Nikoletopoulou et al, 2015;Prasad, 2015;Rai et al, 2015;Denzer et al, 2016;Moos et al, 2016;Suliman and Piantadosi, 2016].…”

Section: Introductionmentioning

confidence: 99%

Epigenetic Treatment of Neurodegenerative Disorders: Alzheimer and Parkinson Diseases

Irwin

Moos

Faller

et al. 2016

Drug Development Research

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Preclinical Research In this review, we discuss epigenetic-driven methods for treating neurodegenerative disorders associated with mitochondrial dysfunction, focusing on carnitinoid antioxidant-histone deacetylase inhibitors that show an ability to reinvigorate synaptic plasticity and protect against neuromotor decline in vivo. Aging remains a major risk factor in patients who progress to dementia, a clinical syndrome typified by decreased mental capacity, including impairments in memory, language skills, and executive function. Energy metabolism and mitochondrial dysfunction are viewed as determinants in the aging process that may afford therapeutic targets for a host of disease conditions, the brain being primary in such thinking. Mitochondrial dysfunction is a core feature in the pathophysiology of both Alzheimer and Parkinson diseases and rare mitochondrial diseases. The potential of new therapies in this area extends to glaucoma and other ophthalmic disorders, migraine, Creutzfeldt-Jakob disease, post-traumatic stress disorder, systemic exertion intolerance disease, and chemotherapy-induced cognitive impairment. An emerging and hopefully more promising approach to addressing these hard-to-treat diseases leverages their sensitivity to activation of master regulators of antioxidant and cytoprotective genes, antioxidant response elements, and mitophagy. Drug Dev Res 77 : 109-123, 2016. © 2016 Wiley Periodicals, Inc.

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Mitochondrial Quality Control as a Therapeutic Target

Cited by 231 publications

References 366 publications

The Role of BCL-2 Family Members in Acute Kidney Injury

The Role of BCL-2 Family Members in Acute Kidney Injury

Effect of Mst1 on Endometriosis Apoptosis and Migration: Role of Drp1-Related Mitochondrial Fission and Parkin-Required Mitophagy

Epigenetic Treatment of Neurodegenerative Disorders: Alzheimer and Parkinson Diseases

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