Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Jha, Saurabh Kumar; Jha, Niraj Kumar; Kumar, Dhiraj; Ambasta, Rashmi K.; Kumar, Pravir

doi:10.1016/j.bbadis.2016.06.015

Cited by 122Mitochondrial Function and PathologyAutophagy in Disease and TherapyAlzheimer's disease research and treatments

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

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Jha, Saurabh Kumar, Jha, Niraj Kumar, Kumar, Dhiraj, Ambasta, Rashmi K., Kumar, Pravir·2017·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

DOI 10.1016/j.bbadis.2016.06.015

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Abstract

Mounting evidence suggests a link between metabolic syndrome (MetS) such as diabetes, obesity, non-alcoholic fatty liver disease in the progression of Alzheimer's disease (AD), Parkinson's disease (PD) and other neurodegenerative diseases (NDDs). For instance, accumulated Aβ oligomer is enhancing neuronal Ca 2+ release and neural NO where increased NO level in the brain through post translational modification is modulating the level of insulin production. It has been further confirmed that irrespective of origin; brain insulin resistance triggers a cascade of the neurodegeneration phenomenon which can be aggravated by free reactive oxygen species burden, ER stress, metabolic dysfunction, neuorinflammation, reduced cell survival and altered lipid metabolism. Moreover, several studies confirmed that MetS and diabetic sharing common mechanisms in the progression of AD and NDDs where mitochondrial dynamics playing a critical role. Any mutation in mitochondrial DNA, exposure of environmental toxin, high-calorie intake, homeostasis imbalance, glucolipotoxicity is causative factors for mitochondrial dysfunction. These cumulative pleiotropic burdens in mitochondria leads to insulin resistance, increased ROS production; enhanced stress-related enzymes that is directly linked MetS and diabetes in neurodegeneration. Since, the linkup mechanism between mitochondrial dysfunction and disease phenomenon of both MetS and NDDs is quite intriguing, therefore, it is pertinent for the researchers to identify and implement the therapeutic interventions for targeting MetS and NDDs. Herein, we elucidated the pertinent role of MetS induced mitochondrial dysfunction in neurons and their consequences in NDDs. Further, therapeutic potential of well-known biomolecules and chaperones to target altered mitochondria has been comprehensively documented. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.

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Our findings report transcriptomic, epigenetic, proteomic, and metabolomic patterns consistent with mitochondrial stress in different cells and multiple organs, including muscle tissues.
“Our findings report transcriptomic, epigenetic, proteomic, and metabolomic patterns (Figs. 2 and 3) consistent with mitochondrial stress in different cells and multiple organs, including muscle tissues (Jha et al., 2017; Topf et al., 2019).”
From Comprehensive Multi-omics Analysis Reveals Mitochondrial Stress as a Central Biological Hub for Spaceflight Impact (2020) · cites this paper as Jha et al., 2017
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Authors: Jha, S. K., Jha, N. K., Kumar, D., Ambasta, R. K., & Kumar, P.
Affiliations: Delhi Technological University (IN)
Corresponding author: Kumar, Pravir
ORCID: Jha, Saurabh Kumar
Jha, Niraj Kumar
Kumar, Dhiraj
Ambasta, Rashmi K.
Kumar, Pravir
Venue: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Publisher: Elsevier BV
Published: 2017-05
Volume: 1863
Issue: 5
Pages: 1132-1146
ISSN: 0925-4439 (ISSN-L)
DOI: 10.1016/j.bbadis.2016.06.015
OpenAlex: W2465261455
Cited by: 122
References: 201
Citations by year: 2026: 12 · 2025: 12 · 2024: 16 · 2023: 10 · 2022: 9 · 2021: 16 · 2020: 18 · 2019: 13 · 2018: 4 · 2017: 11
FWCI: 4.82
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 365 d)
Locations: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
PubMed (publishedVersion)
Funders: Delhi Technological University
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Keywords: mitochondrial dysfunction, metabolic syndrome, neurodegeneration, insulin resistance, reactive oxygen species, endoplasmic reticulum stress, neuroinflammation, Alzheimer's disease, mitochondrial dynamics, mitochondrial DNA mutations, glucolipotoxicity, nitric oxide, stress signaling, mitochondrial chaperone, lipid metabolism
MeSH terms: Animals, Humans, Mitochondria, Reactive Oxygen Species, Neurodegenerative Diseases, Metabolic Syndrome, Endoplasmic Reticulum Stress

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Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

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