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Mitochondria in Health and Disease
- Source :
- Indonesian Biomedical Journal, Vol 11, Iss 1, Pp 1-15 (2019)
- Publication Year :
- 2019
- Publisher :
- Secretariat of The Indonesian Biomedical Journal, 2019.
-
Abstract
- BACKGROUND: Mitochondrial dysfunction known to be associated with most of human inherited disorders and diseases, including neurodegenerative disorders, cardiomyopathies, metabolic syndrome, muscle weakness, cancer, also obesity. CONTENT: Mitochondria charges for multiple anabolic and catabolic circuitries, as the main provider for adenosine triphosphate (ATP). Mitochondria also responsible for cellwide stress responses and control non-apoptotic cell death routines, such as autophagy and regulated necrosis. In other words, mitochondria play an extended role in regulating cellular functions, both vital and lethal, from physiological metabolism to stress responses and death to maintain adult tissue homeostasis. Furthermore, mitochondria are crucial for both embryonic and postembryonic development. Therefore, any defect or alteration in mitochondria signaling pathways will lead to a large number of diseases in human, including premature aging, neurodegenerative disorders, muscle weakness, cardiovascular disorders, and cancer. SUMMARY: Mitochondria perform a dynamic, integrated interconnected network, to maintain tissue homeostasis, beyond the cell boundaries and regulating cells and tissues communication. Certainly any mitochondrial dysfunction could direct to neurodegenerative diseases and metabolic disorders. KEYWORDS: mitochondria, UPR, mitochondrial quality control, proteostasis, mitohormesis, mitochondrial diseases
- Subjects :
- Medicine (General)
R5-920
Subjects
Details
- Language :
- English
- ISSN :
- 20853297 and 23559179
- Volume :
- 11
- Issue :
- 1
- Database :
- Directory of Open Access Journals
- Journal :
- Indonesian Biomedical Journal
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.897cbaa382e942b4a0f4f05058de3a18
- Document Type :
- article
- Full Text :
- https://doi.org/10.18585/inabj.v11i1.779