Understanding Age-Related Muscle Loss: The Role of Mitochondrial DNA Mutations
- December 25, 2024
- Posted by: OptimizeIAS Team
- Category: DPN Topics
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Understanding Age-Related Muscle Loss: The Role of Mitochondrial DNA Mutations
Sub: Sci
Sec: Health
Why in News
- Recent research published in the journal Genome Research by scientists from the University of California Los Angeles and the University of Alberta, Canada, reveals a significant link between mitochondrial DNA (mtDNA) deletion mutations and biological aging. This study sheds light on why humans lose muscle mass with age and offers insights into the mechanisms underlying this process.
Mitochondrial DNA and Aging:
- As humans age, deletion mutations in mtDNA accumulate, particularly in tissues like skeletal muscle and the brain. These mutations impair mitochondrial function, leading to cell death and muscle mass loss.
About Mitochondrial DNA:
- The nuclear genome comprises approximately 3.2 billion base pairs and encodes 20,000 protein-coding genes.
- In contrast, the mtDNA is much smaller, consisting of 16,569 base pairs and encoding 13 protein-coding genes.
- Mitochondria are inherited exclusively from the mother’s egg.
- Mitochondria evolved from free-living bacteria that became symbiotic with early single-celled organisms.
- Over time, most mitochondrial genes were transferred to the nuclear genome, leaving only a small subset in the mtDNA.
- Importance of Mitochondria: Mitochondria are known as the “powerhouses of the cell” because they synthesize adenosine triphosphate (ATP), the primary energy source for cellular functions.
- Mitochondria have their own genome (mtDNA), which encodes essential proteins for their function.
Mechanisms Behind Muscle Loss:
- Deletion mutations involve the loss of thousands of base pairs from mtDNA, resulting in smaller, mutated mtDNA molecules. These defective mtDNA molecules outcompete normal mtDNA during cell replication, disrupting mitochondrial function.
- Deletion mutations can bring together sequences of different mtDNA genes, creating novel “chimeric” genes. These chimeric genes interfere with the normal function of mtDNA, exacerbating mitochondrial dysfunction.
- When too many mtDNA molecules are damaged, mitochondria fail to produce sufficient ATP, causing muscle cells to lose their ability to contract and eventually die. This process underpins age-related muscle mass loss.