Study of Mitochondrial Dysfunction Using Genome and Transcriptome Analysis
A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".
Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 1447
Special Issue Editor
Interests: PCR; DNA; gel electrophoresis; molecular cloning; cell culture; gene expression; electrophoresis; atherosclerosis; cell biology; genetics; biotechnology
Special Issue Information
Dear Colleagues,
According to the literature data, in human pathology, the association of various diseases with some mitochondrial genome mutations has been shown. Mitochondrial mutations are associated with different pathologies, such as atherosclerosis, coronary artery stenosis, some forms of diabetes and deafness, susceptibility to acute myocardial infarction, and cardiomyopathy. Human mitochondrial DNA is a circular double-stranded molecule. Each mitochondrion contains several copies of its genome. The mitochondrial genome is maternally inherited. It is characterized by pronounced instability; therefore, somatic mutations that occur during the life of an individual are not uncommon. Penetrance and expressivity of such mutations vary widely between relatives (on the maternal side) from family to family and depend on many factors, but mainly on the genotype and the level of heteroplasmy (a mixture of mutant and normal DNA molecules). Damage of mitochondria can contribute to the development of energy deficiency in a cell, the activation of free radical processes, and the initiation of mechanisms of programmed cell death. Disorders in mitochondrial functions include a universal pathological mechanism that is involved in the development of a large number of different pathological processes associated with the production of free radicals and ischemia/reperfusion. Of great interest is the possibility of the indirect influence of mitochondrial dysfunction on the development of diseases in humans, because of the weakening of the body's resistance to pathological processes. For approximately 20 years, we have been studying the role of mitochondrial genome mutations in the occurrence and development of atherosclerotic lesions. We found that these mutations lead to mitochondrial dysfunction in atherosclerosis. We would like to consider the association of mitochondrial dysfunction with human diseases. This Special Issue will be devoted to the study of mitochondrial dysfunction in various human pathologies.
Dr. Margarita A. Sazonova
Guest Editor
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Keywords
- mitochondrial dysfunction
- cellular dysfunction
- human diseases
- mutation
- gene
- mitochondrial genome
- transcriptome
