IMR Press / FBL / Volume 21 / Issue 4 / DOI: 10.2741/4420

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Review

Mitochondrial anomalies: driver to age associated degenerative human ailments

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1 School of Biological Sciences, Dr. H. S. Gour Central University, Sagar, India
2 Division of Translational Research, Tata Memorial Centre, ACTREC, Mumbai, India
Academic Editors:Aditi Mehrotra, Surendra Kumar Trigun, Raj Kumar Koiri, Dharmendra Sharma
Front. Biosci. (Landmark Ed) 2016, 21(4), 769–793;
Published: 1 January 2016
(This article belongs to the Special Issue Frontiers in modern biology)

Mitochondria play a fundamental role in regulating a variety of complex metabolic processes to maintain adequate energy balance for cellular existence. To orchestrate these functions, an undisturbed mitochondrial dynamics is imperative through a set of tightly guided mechanisms. Interference in key signature processes by several genetic, epigenetic and age-linked factors triggers mitochondrial dysfunction through decrease in mitochondrial biogenesis, reduced mitochondrial content, aberrant mtDNA mutations, increased oxidative stress, deficient mitophagy, energy dysfunction, decrease in anti oxidant defense and impaired calcium homeostasis. Mitochondrial dysfunction is widely implicated in origin and development of various age associated degenerative human ailments including metabolic syndromes, cardiovascular diseases, cancer, diabetes and neurodegenerative disorders. The present review revisits the mitochondrial anomalies involved in aetiology of different human diseases and also highlights the translational significance of nano-vectors aimed for selective mitochondrial engineering which might pave way for development of novel therapeutics.

Mitochondrial Dysfunction
Oxidative Stress
Oxidative Damage
Redox Signaling
Mitochondria Targeting
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