Literature DB >> 25711915

Mitochondria in health, aging and diseases: the epigenetic perspective.

Patrizia D'Aquila1, Dina Bellizzi, Giuseppe Passarino.   

Abstract

The rate/quality of human aging and the development/progression of diseases depend on a complex interplay among genetics, epigenetics and environment. In this scenario, mitochondrial function (or dysfunction) and mitochondrial DNA have emerged as major players. This is mainly due to their crucial role in energetic balance, in modulating epigenetic programs and in influencing cell stress response. Moreover, it is also emerging the existence of epigenetic changes in mitochondrial DNA and of non coding mitochondrial RNAs which, together with the nuclear ones, play regulatory roles in numerous human phenotypes. In this review we will provide an overview on "mitochondrial epigenetics" state of the art, by summarizing the involvement of mitochondrial function and of mitochondria-nucleus communication in regulating nuclear epigenome, as well as the key aspects of the epigenetic marks related to mitochondrial DNA. Despite the limited data available in the literature to date, mainly due to the novelty of the topic, the intriguing interplay of the mitochondrial epigenetic changes in both physiological and pathological conditions will also be presented.

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Year:  2015        PMID: 25711915     DOI: 10.1007/s10522-015-9562-3

Source DB:  PubMed          Journal:  Biogerontology        ISSN: 1389-5729            Impact factor:   4.277


  23 in total

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8.  Genomic deletion of GIT2 induces a premature age-related thymic dysfunction and systemic immune system disruption.

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10.  Humanin G (HNG) protects age-related macular degeneration (AMD) transmitochondrial ARPE-19 cybrids from mitochondrial and cellular damage.

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