Mitochondria: Metabolic “Engine” of the Cell and Redox Signaling in Human Diseases
A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".
Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 457
Special Issue Editor
2. Technology Commercialization Center, Office of Business Development, Taipei Medical University, Taipei 11031, Taiwan
Interests: mitochondrial disease; metabolic syndrome; metabolic reprogramming; mitochondrial biogenesis; glycolysis; oxidative stress; redox signalings; AMPK; PGC-1α; FOXO3a
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Mitochondria execute a crucial role in energy production, metabolism, and signaling to maintain cellular homeostasis and development. It is well established that mitochondrial dysfunction-elicited reactive oxygen species (ROS) play a vital role in the pathogenesis of mitochondrial diseases, and the expression levels of several clusters of genes are altered in response to the elevated oxidative stress. Further, mitochondrial dysfunction is linked to the pathogenesis and progression of human diseases such as metabolic syndrome, cancer, neurodegenerative diseases, and cardiovascular diseases. Recently, mitochondrial-associated molecular pathways have been reported and are often compromised in the pathophysiology of diseases progression, including the AMPK, PGC1a, Nrf2, and PPARγ and several redox signaling pathways. Impairments to these signaling pathways consequently affect the removal of dysfunctional mitochondria, which has been suggested as contributing to the development of disease. Therefore, the prevention of mitochondrial dysfunction has become an attractive therapeutic target, and there are several molecular pathways that can be pharmacologically targeted to remove damaged mitochondria by inducing mitochondrial biogenesis or mitophagy, as well as increasing the antioxidant capacity in order to alleviate mitochondrial dysfunction and prevent the development and progression in these disorders.
Much work has been carried out to elucidate the impact of mitochondrial dysfunction in human diseases involved in cell and redox signaling. Elucidation of the adaptive mechanism involved in these activation cascades such as AMPK and PGC1a would help us to gain a deeper insight into the crosstalk between mitochondria and the nucleus in the pathogenesis of mitochondrial diseases. However, the precise mitochondrial-associated metabolic and molecular processes in disease progression remain comparatively unknown. Therefore, the alteration of mitochondrial metabolism and metabolic reprograming in human diseases needs further study. This Special Issue is dedicated to research focusing on recent advances in mitochondrial metabolism and redox signaling in human diseases. We will consider original research articles, concept papers, short communications, and reviews on all aspects of mitochondria-associated human diseases. Our aim is for this Special Issue to contribute to advancing this fascinating field.
Dr. Shibei Wu
Guest Editor
Manuscript Submission Information
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Keywords
- Mitochondria
- Mitochondrial biogenesis
- Metabolic reprogramming
- Glycolysis
- Oxidative stress
- Redox signaling
- Adaptive response
- Metabolic disorders
- Mitochondrial disease
- Cancer
- Neurodegenerative
- MtDNA mutation
- AMPK
- PGC-1α
- FOXO3a
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