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In geriatric patients, renal physiology undergoes significant changes, including diminished renal blood flow and a lower glomerular filtration rate (GFR), leading to alterations in medication clearance. Drugs such as aminoglycoside antibiotics, lithium, and digoxin, which rely on glomerular filtration for removal from the body, particularly impact pharmacokinetics. These drugs tend to have slower clearance rates in older adults, necessitating careful dosage considerations.Evaluation of renal...
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Idh2 deficiency accelerates renal dysfunction in aged mice.

Su Jeong Lee1, Hanvit Cha1, Seoyoon Lee1

  • 1School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, College of Natural Sciences, Kyungpook National University, Taegu, South Korea.

Biochemical and Biophysical Research Communications
|September 21, 2017
PubMed
Summary

Mitochondrial NADP+-dependent isocitrate dehydrogenase (IDH2) is crucial for antioxidant defense. IDH2 depletion accelerates aging and kidney degeneration, supporting the oxidative stress theory of aging.

Keywords:
AgingAntioxidant enzymeKnockout miceMitochondriaRedox status

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Area of Science:

  • Mitochondrial biology
  • Aging research
  • Oxidative stress

Background:

  • The free radical theory of aging suggests senescence results from accumulated oxidative damage from reactive oxygen species (ROS).
  • Mitochondrial antioxidant systems rely on the NADPH pool, primarily generated by NADP+-dependent isocitrate dehydrogenase (IDH2).

Purpose of the Study:

  • To investigate the role of IDH2 in aging and oxidative stress.
  • To determine the impact of IDH2 depletion on lifespan and age-related traits in mice.

Main Methods:

  • Mice with IDH2 depletion (idh2-/-) were compared to wild-type mice.
  • Evaluated lifespan, age-sensitive traits (hair, skin, eyes), and kidney function and structure.

Main Results:

  • IDH2 depletion shortened lifespan and accelerated aging phenotypes.
  • Kidney degeneration was uniquely accelerated in idh2-/- mice.
  • Mice lacking IDH2 exhibited pronounced redox status disruption, oxidative damage, and apoptosis.

Conclusions:

  • Compromised mitochondrial antioxidant defenses, specifically IDH2 deficiency, significantly contribute to aging.
  • These findings support the oxidative stress theory of aging, highlighting the kidney as a key organ affected by mitochondrial dysfunction.