Mitochondrial dysfunction due to alterations in mitochondrial DNA (mtDNA) gene expression and replication underlie several human pathologies. However, the exact mechanisms through which these alterations arise are still poorly understood. In recent years, a growing number of studies identified epigenetic mechanisms that act inside mitochondria, thus opening a new filed of research that could provide new knowledge on the mitochondria regulation in both physiological and pathological conditions. Indeed, aberrant mtDNA methylation and altered expression of mtDNA non-coding RNAs have been found in animal models and in human tissues from patients affected by cancer, neurodegenerative and cardiovascular diseases, obesity, and diabetes. Moreover, genetic variants and altered epigenetic regulation of nuclear-encoded mitochondrial genes, as well as environmental factors, are also involved in the dysfunction of mtDNA gene expression and replication through alteration of mitochondrial epigenetic mechanisms. A better understanding of the intricate interplay among nuclear and mitochondria epigenetic alterations that underlie mitochondrial dysfunction could provide new insights into the pathophysiology of human diseases characterized by a mitochondrial impairment.
This Research Topic aims to provide a detailed and updated overview of the genetic and epigenetic changes inducing mitochondrial dysfunction in human diseases. We welcome research and review articles covering studies in human samples, cell cultures, and animal models of human diseases characterized by mitochondrial dysfunction. Basic research articles aimed to identify mitochondrial dysfunction-related genetics and epigenetic biomarkers of human diseases, as well as research papers dealing with the potential of therapeutic approaches targeting mitochondrial alteration in these conditions, are also well accepted.
Updated reviews are more than welcome, as well as systematic reviews of the literature or mini-review articles addressing a specific theme. We are also interested in articles addressing the contribution of environmental or early-life factors to the alteration of mitochondrial biology observed in these conditions. This topic is also opened to methodological papers, as well as papers addressing the clinical utility of epigenetic investigations in these disorders.
This collection aims to provide a detailed and updated overview of the genetic variants and epigenetic alterations that induce a mitochondrial dysfunction in human diseases.
We are interested in:
• Articles on genetic and epigenetic biomarkers related to mitochondrial dysfunction in human complex diseases;
• Articles addressing the clinical utility of genetic and epigenetic biomarkers related to mitochondrial dysfunction in human diseases;
• Articles addressing the potential therapeutic opportunities of targeting these biomarkers;
• Articles linking epi-genetic biomarkers, environmental or early-life events to mitochondrial dysfunction in human diseases;
• Either candidate-gene studies or genome-wide approaches are welcome;
• Narrative Reviews, Systematic Reviews, Mini Reviews;
• Research papers, Methodological papers, Short communications.
Mitochondrial dysfunction due to alterations in mitochondrial DNA (mtDNA) gene expression and replication underlie several human pathologies. However, the exact mechanisms through which these alterations arise are still poorly understood. In recent years, a growing number of studies identified epigenetic mechanisms that act inside mitochondria, thus opening a new filed of research that could provide new knowledge on the mitochondria regulation in both physiological and pathological conditions. Indeed, aberrant mtDNA methylation and altered expression of mtDNA non-coding RNAs have been found in animal models and in human tissues from patients affected by cancer, neurodegenerative and cardiovascular diseases, obesity, and diabetes. Moreover, genetic variants and altered epigenetic regulation of nuclear-encoded mitochondrial genes, as well as environmental factors, are also involved in the dysfunction of mtDNA gene expression and replication through alteration of mitochondrial epigenetic mechanisms. A better understanding of the intricate interplay among nuclear and mitochondria epigenetic alterations that underlie mitochondrial dysfunction could provide new insights into the pathophysiology of human diseases characterized by a mitochondrial impairment.
This Research Topic aims to provide a detailed and updated overview of the genetic and epigenetic changes inducing mitochondrial dysfunction in human diseases. We welcome research and review articles covering studies in human samples, cell cultures, and animal models of human diseases characterized by mitochondrial dysfunction. Basic research articles aimed to identify mitochondrial dysfunction-related genetics and epigenetic biomarkers of human diseases, as well as research papers dealing with the potential of therapeutic approaches targeting mitochondrial alteration in these conditions, are also well accepted.
Updated reviews are more than welcome, as well as systematic reviews of the literature or mini-review articles addressing a specific theme. We are also interested in articles addressing the contribution of environmental or early-life factors to the alteration of mitochondrial biology observed in these conditions. This topic is also opened to methodological papers, as well as papers addressing the clinical utility of epigenetic investigations in these disorders.
This collection aims to provide a detailed and updated overview of the genetic variants and epigenetic alterations that induce a mitochondrial dysfunction in human diseases.
We are interested in:
• Articles on genetic and epigenetic biomarkers related to mitochondrial dysfunction in human complex diseases;
• Articles addressing the clinical utility of genetic and epigenetic biomarkers related to mitochondrial dysfunction in human diseases;
• Articles addressing the potential therapeutic opportunities of targeting these biomarkers;
• Articles linking epi-genetic biomarkers, environmental or early-life events to mitochondrial dysfunction in human diseases;
• Either candidate-gene studies or genome-wide approaches are welcome;
• Narrative Reviews, Systematic Reviews, Mini Reviews;
• Research papers, Methodological papers, Short communications.
