scholarly journals Editorial: Role of Mitochondrial Quality Control in Myocardial and Microvascular Physiology and Pathophysiology

2021 ◽  
Vol 12 ◽  
Author(s):  
Amanda Lochner ◽  
Hsueh-Hsiao Wang ◽  
Russel J. Reiter ◽  
Rui Guo ◽  
Hao Zhou
Keyword(s):  
Quality Control ◽  
Mitochondrial Quality Control

scholarly journals Role of the ISR-ATF4 pathway and its cross talk with Nrf2 in mitochondrial quality control

2019 ◽  
Vol 64 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Shuya Kasai ◽  
Hiromi Yamazaki ◽  
Kunikazu Tanji ◽  
Máté János Engler ◽  
Tomoh Matsumiya ◽  
...  
Keyword(s):  
Quality Control ◽  
Cross Talk ◽  
Mitochondrial Quality Control

Mitochondrial Quality Control and Restraining Innate Immunity

2020 ◽  
Vol 36 (1) ◽  
pp. 265-289
Author(s):  
Andrew T. Moehlman ◽  
Richard J. Youle
Keyword(s):  
Innate Immunity ◽  
Quality Control ◽  
Neurodegenerative Diseases ◽  
Innate Immune ◽  
Interferon Response ◽  
Mitochondrial Quality Control ◽  
Selective Autophagy ◽  
Eukaryotic Organisms ◽  
And Function

Maintaining mitochondrial health is essential for the survival and function of eukaryotic organisms. Misfunctioning mitochondria activate stress-responsive pathways to restore mitochondrial network homeostasis, remove damaged or toxic proteins, and eliminate damaged organelles via selective autophagy of mitochondria, a process termed mitophagy. Failure of these quality control pathways is implicated in the pathogenesis of Parkinson's disease and other neurodegenerative diseases. Impairment of mitochondrial quality control has been demonstrated to activate innate immune pathways, including inflammasome-mediated signaling and the antiviral cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING)–regulated interferon response. Immune system malfunction is a common hallmark in many neurodegenerative diseases; however, whether inflammation suppresses or exacerbates disease pathology is still unclear. The goal of this review is to provide a historical overview of the field, describe mechanisms of mitochondrial quality control, and highlight recent advances on the emerging role of mitochondria in innate immunity and inflammation.

scholarly journals Stanniocalcin-1 Alleviates Contrast-Induced Acute Kidney Injury by Regulating Mitochondrial Quality Control via the Nrf2 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-17 ◽  
Author(s):  
Fei Zhao ◽  
Li-Xin Feng ◽  
Qian Liu ◽  
Hong-Shen Wang ◽  
Cheng-Yuan Tang ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Quality Control ◽  
Kidney Injury ◽  
Protective Role ◽  
Mitochondrial Quality Control ◽  
Therapy Strategy ◽  
Nrf2 Signaling Pathway ◽  
Short And Long Term ◽  
Renal Tubular

Contrast-induced acute kidney injury (CI-AKI) is the third common cause of acute kidney injury (AKI), which is associated with poor short- and long-term outcomes. Currently, effective therapy strategy for CI-AKI remains lacking. Stanniocalcin-1 (STC1) is a conserved glycoprotein with antiapoptosis and anti-inflammatory functions, but the role of STC1 in controlling CI-AKI is unknown. Here, we demonstrated a protective role of STC1 in contrast-induced injury in cultured renal tubular epithelial cells and CI-AKI rat models. Recombinant human STC1 (rhSTC1) regulated mitochondrial quality control, thus suppressing contrast-induced mitochondrial damage, oxidative stress, inflammatory response, and apoptotic injury. Mechanistically, activation of the Nrf2 signaling pathway contributes critically to the renoprotective effect of STC1. Together, this study demonstrates a novel role of STC1 in preventing CI-AKI and reveals Nrf2 as a molecular target of STC1. Therefore, this study provides a promising preventive target for the treatment of CI-AKI.

scholarly journals The role of GABARAPL1/GEC1 in Autophagic Flux and Mitochondrial Quality Control in MDA-MB-436 Breast Cancer Cells

2017 ◽  
Vol 112 ◽  
pp. 107-108 ◽  
Author(s):  
Michael Boyer-Guittaut ◽  
Sooryanarayana Varambally ◽  
Victor Darley-Usmar ◽  
Jianhua Zhang
Keyword(s):  
Breast Cancer ◽  
Quality Control ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Autophagic Flux ◽  
Mitochondrial Quality Control

scholarly journals The Role of Posttranslational Modification and Mitochondrial Quality Control in Cardiovascular Diseases

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Jinlin Liu ◽  
Li Zhong ◽  
Rui Guo
Keyword(s):  
Quality Control ◽  
Posttranslational Modifications ◽  
Posttranslational Modification ◽  
Protein Function ◽  
Therapeutic Potential ◽  
Normal Function ◽  
Future Research ◽  
Mitochondrial Quality Control ◽  
Mitochondrial Homeostasis

Cardiovascular disease (CVD) is the leading cause of death in the world. The mechanism behind CVDs has been studied for decades; however, the pathogenesis is still controversial. Mitochondrial homeostasis plays an essential role in maintaining the normal function of the cardiovascular system. The alterations of any protein function in mitochondria may induce abnormal mitochondrial quality control and unexpected mitochondrial dysfunction, leading to CVDs. Posttranslational modifications (PTMs) affect protein function by reversibly changing their conformation. This review summarizes how common and novel PTMs influence the development of CVDs by regulating mitochondrial quality control. It provides not only ideas for future research on the mechanism of some types of CVDs but also ideas for CVD treatments with therapeutic potential.

scholarly journals mSphere of Influence: Role of IRGM1 in Disease Control

mSphere ◽  
2021 ◽  
Vol 6 (2) ◽  
Author(s):  
Sumanta Kumar Naik
Keyword(s):  
Immune Response ◽  
Quality Control ◽  
Mycobacterium Tuberculosis ◽  
Immune Responses ◽  
Disease Control ◽  
Host Immune Response ◽  
Specific Interest ◽  
Mitochondrial Quality Control ◽  
Content Type

ABSTRACT Sumanta K. Naik works in the tuberculosis field, with a specific interest in the host immune response to Mycobacterium tuberculosis infection. In this mSphere of Influence article, he reflects on how the paper “IRGM1 links mitochondrial quality control to autoimmunity” by Prashant Rai et al. (Nat Immunol, 22:312–321, 2021, https://doi.org/10.1038/s41590-020-00859-0) impacted his research by revealing new roles for Irgm1 in immune responses.

scholarly journals PINK1 deficiency impairs osteoblast differentiation through aberrant mitochondrial homeostasis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
So-Young Lee ◽  
Hyun-Ju An ◽  
Jin Man Kim ◽  
Min-Ji Sung ◽  
Do Kyung Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Quality Control ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Quality Control ◽  
Mitochondrial Homeostasis ◽  
Ovariectomized Mice ◽  
Species Production

Abstract Background PTEN-induced kinase 1 (PINK1) is a serine/threonine-protein kinase in mitochondria that is critical for mitochondrial quality control. PINK1 triggers mitophagy, a selective autophagy of mitochondria, and is involved in mitochondrial regeneration. Although increments of mitochondrial biogenesis and activity are known to be crucial during differentiation, data regarding the specific role of PINK1 in osteogenic maturation and bone remodeling are limited. Methods We adopted an ovariectomy model in female wildtype and Pink1−/− mice. Ovariectomized mice were analyzed using micro-CT, H&E staining, Masson’s trichrome staining. RT-PCR, western blot, immunofluorescence, alkaline phosphatase, and alizarin red staining were performed to assess the expression of PINK1 and osteogenic markers in silencing of PINK1 MC3T3-E1 cells. Clinical relevance of PINK1 expression levels was determined via qRT-PCR analysis in normal and osteoporosis patients. Results A significant decrease in bone mass and collagen deposition was observed in the femurs of Pink1−/− mice after ovariectomy. Ex vivo, differentiation of osteoblasts was inhibited upon Pink1 downregulation, accompanied by impaired mitochondrial homeostasis, increased mitochondrial reactive oxygen species production, and defects in mitochondrial calcium handling. Furthermore, PINK1 expression was reduced in bones from patients with osteoporosis, which supports the practical role of PINK1 in human bone disease. Conclusions In this study, we demonstrated that activation of PINK1 is a requisite in osteoblasts during differentiation, which is related to mitochondrial quality control and low reactive oxygen species production. Enhancing PINK1 activity might be a possible treatment target in bone diseases as it can promote a healthy pool of functional mitochondria in osteoblasts.

Emerging Role of Mitophagy in Inflammatory Diseases: Cellular and Molecular Episodes

2020 ◽  
Vol 26 (4) ◽  
pp. 485-491 ◽  
Author(s):  
Mohamed Adil A.A. ◽  
Shabnam Ameenudeen ◽  
Ashok Kumar ◽  
S. Hemalatha ◽  
Neesar Ahmed ◽  
...  
Keyword(s):  
Quality Control ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Inflammatory Diseases ◽  
Mitochondrial Quality Control ◽  
Mitochondrial Injury ◽  
Cellular Events ◽  
Evolutionarily Conserved

Mitochondria are the crucial regulators for the major source of ATP for different cellular events. Due to damage episodes, mitochondria have been established for a plethora ofalarming signals of stress that lead to cellular deterioration, thereby causing programmed cell death. Defects in mitochondria play a key role in arbitrating pathophysiological machinery with recent evince delineating a constructive role in mitophagy mediated mitochondrial injury. Mitophagy has been known for the eradication of damaged mitochondria via the autophagy process. Mitophagy has been investigated as an evolutionarily conserved mechanism for mitochondrial quality control and homeostasis. Impaired mitophagy has been critically linked with the pathogenesis of inflammatory diseases. Nevertheless, the exact mechanism is not quite revealed, and it is still debatable. The purpose of this review was to investigate the possible role of mitophagy and its associated mechanism in inflammation-mediated diseases at both the cellular and molecular levels.

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