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Updated: Feb 2, 2026

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Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence
Published on: May 22, 2013
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Klotho Deficiency Accelerates Stem Cells Aging by Impairing Telomerase Activity.
Mujib Ullah1,2, Zhongjie Sun1,3
1Department of Physiology, College of Medicine, University of Oklahoma Health Sciences Center, Biomedical Research Center, Oklahoma City.
Summary
Klotho deficiency accelerates stem cell aging by impairing telomerase activity and telomere length. Cycloastragenol partially restored telomerase, indicating Klotho
Area of Science:
- Gerontology and Stem Cell Biology
- Molecular Mechanisms of Aging
Background:
- Aging involves stem cell functional decline.
- Klotho (KL) is an antiaging protein linked to extended lifespan.
- The role of KL deficiency in stem cell aging requires elucidation.
Purpose of the Study:
- To investigate if Klotho deficiency accelerates stem cell aging and telomere shortening.
- To identify mechanisms linking KL deficiency to stem cell dysfunction.
- To assess cycloastragenol's efficacy in restoring telomerase activity in aged stem cells.
Main Methods:
- Klotho knockdown using siRNA.
- Assessment of telomerase activity, differentiation potential, pluripotency, senescence, and apoptosis.
- Analysis of gene expression (TERF1, TERT, POT1, TGFβ1, CD90, bFGF).
- Evaluation of cycloastragenol treatment effects.
Main Results:
- Klotho deficiency diminished telomerase activity and altered TERF1 and TERT expression.
- KL deficiency impaired stem cell differentiation, pluripotency, and induced senescence and apoptosis.
- Telomerase activity decreased with KL knockdown.
- Cycloastragenol partially rescued telomerase deterioration.
Conclusions:
- Klotho deficiency accelerates stem cell aging via reduced telomerase activity and telomere shortening.
- KL and telomeres regulate stem cell aging through TERF1, POT1, and TERT, influenced by TGFβ, Insulin, and Wnt signaling.
- KL plays a critical role in life extension by regulating telomere length and telomerase activity.
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