Mitochondrial Dysfunction in Aging and Metabolic Diseases II
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".
Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 1472
Special Issue Editors
Interests: mitochondrial dysfunction; cardiolipin remodeling; aging; metabolic diseases
Special Issues, Collections and Topics in MDPI journals
Interests: aging; mitochondrial dysfunction; cardiolipin remodeling; mitophagy; mitochondrial transport; innate immune response
Special Issue Information
Dear Colleagues,
Mitochondria are crucial for cellular bioenergetics and play a major role in multiple cellular processes that dictate the fate of a cell. Mitochondrial dysfunction is characterized by a reduced efficiency of oxidative phosphorylation, the generation of free radicals, and reductions in the synthesis of adenosine-5′-triphosphate. Accumulating evidence has suggested that mitochondrial dysfunction plays a critical role in the pathogenesis of aging and age-related metabolic diseases, including type 2 diabetes, obesity, cardiovascular diseases, and neurodegenerative diseases. Mitochondria undergo periodical cycles of fission, fusion, and mitophagy as quality control processes. Defects in such a process cause the accumulation of damaged mitochondria, which in turn decreases oxidative phosphorylation and increases the production of reactive oxygen species. Moreover, mitochondrial DNA (mtDNA) mutations increase in frequency with age, and increased levels of mtDNA mutations also contribute to the onset of aging and age-related diseases. In addition, emerging evidence suggests that mitochondrial phospholipids, such as cardiolipin (CL) and phosphatidylglycerol (PG), play a pivotal role in maintaining mitochondrial integrity and function. Accordingly, mitochondrial membrane phospholipid compositions are directly linked to metabolic rate and life span in a wide variety of animal species. Furthermore, CL is highly prone to oxidative damage by free radicals due to its exclusive location in the mitochondrial membranes where reactive oxygen species are generated. Oxidized CL not only causes mitochondrial dysfunction, but also activates several innate immune pathways, leading to chronic inflammation and cellular senescence in aging and age-related metabolic diseases. Although the underlying molecular pathways in regulating mitochondrial function are complex, it is crucial to understand the nexus of mitochondrial dysfunction in aging and age-related metabolic diseases.
The current Special Issue will accept original studies, reviews, and technical reports in the field of mitochondrial biology and dysfunction, including mitochondrial quality control, oxidative stress, mtDNA integrity, synthesis, and the remodeling of mitochondrial phospholipids in aging and age-related metabolic diseases, written by scientists active in the field.
Dr. Yuguang Shi
Dr. Jun Zhang
Guest Editors
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Keywords
- mitochondrial dysfunction
- aging
- metabolic diseases
- oxidative stress
- mitophagy
- mtDNA
- cellular senescence
- mitochondrial phospholipids
- cardiolipin
- mitochondrial protein and lipid transport
- mitochondrial dynamics
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Related Special Issue
- Mitochondrial Dysfunction in Aging and Metabolic Diseases in Cells (5 articles)
