IMR Press / FBL / Special Issues / 1326789875768655874

Cellular response to mitochondrial dysfunction and pathogenic mtDNA mutations

Submission deadline: 31 January 2022
Special Issue Editor
  • Yau-Huei Wei
    Center for Mitochondrial Medicine and Free Radical Research, Changhua Christian Hospital, Changhua City, Taiwan 50046
    Interests: Mitochondrial Disease; Mitochondrial DNA Mutation; Stem Cells; iPSC; Metabolic Reprogramming
Special Issue Information

Dear Colleagues,

Mitochondrial DNA (mtDNA) mutations result in not only inefficient supply of ATP but also increased production of reactive oxygen species (ROS) such as superoxide anions and hydrogen peroxide in mitochondria of the affected tissues of patients with mitochondrial disease or in elderly subjects. Extensive studies have demonstrated that such an increase of oxidative stress contributes to alterations in the gene expression and activities of enzymes in several metabolic pathways. Several antioxidant enzymes are altered and oxidative damage to DNA, RNA, proteins, and lipids are increased in tissues and cultured cells from mitochondrial disease patients or elderly subjects. The changes at the protein and activity levels of several metabolic pathways result in metabolic reprogramming, which plays an important role in adaptive response and survival of human cells harboring a pathogenic mtDNA mutation. This special issue is focused on the molecular mechanism and consequences of human cell response to pathogenic mtDNA mutation and/or mitochondrial dysfunction.

Prof. Dr. Yau-Huei Wei

Guest Editor

Keywords
Mitochondrial DNA Mutation
Mitochondrial Dysfunction
Mitochondrial Disease
Mitophagy
Oxidative Stress
Manuscript Submission Information

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Published Paper (9 Papers)
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