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Related Concept Videos

Mismatch Repair01:20

Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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DNA Distortion and Damage
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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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Related Experiment Video

Updated: Aug 1, 2025

Methods to Study Changes in Inherent Protein Aggregation with Age in Caenorhabditis elegans
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Mitigating age-related somatic mutation burden.

Jan Vijg1, Björn Schumacher2, Abdulkadir Abakir3

  • 1Department of Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA; Center for Single-Cell Omics, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

Trends in Molecular Medicine
|April 30, 2023
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Summary
This summary is machine-generated.

Somatic mutations accumulate in our bodies due to DNA repair errors, potentially driving aging. Research explores quantifying these mutations and strategies to prevent them, aiming to extend healthspan.

Keywords:
agingcancerchromatin organizationclonal hematopoiesisgermline versus somatic genomesomatic mutations

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Area of Science:

  • Genetics
  • Molecular Biology
  • Gerontology

Background:

  • Genomes require constant DNA repair for stability.
  • Repair mechanisms are optimized for reproduction, not long-term integrity.
  • Somatic mutations accumulate in tissues with age.

Purpose of the Study:

  • Review advances in quantitative analysis of somatic mutations in vivo.
  • Evaluate the causal role of somatic mutations in aging.
  • Discuss strategies to prevent or delay somatic mutations as a cause of aging.

Main Methods:

  • Quantitative analysis of somatic mutations.
  • Review of existing evidence on somatic mutations and aging.
  • Discussion of preventative strategies.

Main Results:

  • Somatic mutations are confirmed to accumulate in human and model organism tissues.
  • Evidence for and against a causal link between somatic mutations and aging is reviewed.
  • Potential strategies for preventing de novo somatic mutations are discussed.

Conclusions:

  • Somatic mutations are a significant factor in aging.
  • Further research into quantitative analysis and prevention is warranted.
  • Interventions targeting somatic mutations may offer a path to delay aging.