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Inducing Energetic Switching Using Klotho Improves Vascular Smooth Muscle Cell Phenotype.

Craig K Docherty1, Anastasiya Strembitska1, Christa P Baker1

  • 1Institute of Cardiovascular and Medical Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, University Avenue, Glasgow G12 8TA, UK.

International Journal of Molecular Sciences
|January 11, 2022
PubMed
Summary
This summary is machine-generated.

The anti-aging protein Klotho enhances vascular smooth muscle cell (VSMC) survival in atherosclerosis by improving energy metabolism. This discovery offers a potential strategy to delay plaque rupture and reduce heart attack and stroke risks.

Keywords:
glycolysismitochondrial ATP generationmitochondrial dysfunctionoxidative metabolismvascular smooth muscle cells

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Area of Science:

  • Cardiovascular Disease Research
  • Cellular Metabolism
  • Aging Biology

Background:

  • Atherosclerosis is characterized by aged vascular smooth muscle cells (VSMCs) and impaired cell survival.
  • Key markers include DNA damage (p53, ATM) and mitochondrial dysfunction in plaques.
  • The anti-aging protein Klotho shows potential to enhance VSMC survival and delay plaque rupture.

Purpose of the Study:

  • To investigate the role of Klotho in VSMC survival and energy metabolism in atherosclerosis.
  • To compare the effects of Klotho in wild-type VSMCs versus those with mitochondrial dysfunction (Pink1 knockout).

Main Methods:

  • Screening of wild-type ApoE VSMCs for drug candidates promoting longevity without cytotoxicity.
  • Assessment of AMP Kinase (AMPK) as a readout for energy homeostasis.
  • Evaluation of metabolic switching (oxidative vs. glycolytic) using XF24 technology and live cell imaging, comparing WT and Pink1 knockout cells.

Main Results:

  • Klotho was selected for its ability to mediate energetic switching between oxidative and glycolytic metabolism.
  • Klotho improved glycolytic energetics and cell survival, migration, and proliferation in wild-type VSMCs.
  • These benefits were absent in Pink1 knockout cells, highlighting the necessity of functional mitochondria.

Conclusions:

  • Klotho plays a critical role in VSMC energetics, requiring Pink1 for metabolic switching.
  • Klotho improves VSMC phenotype and survival, offering a potential therapeutic strategy for atherosclerosis.
  • Early targeting of Klotho to atherosclerotic plaques could delay disease progression and reduce cardiovascular events.