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Pck1 Deficiency Drives Mitochondrial Dysfunction and Cellular Senescence in Adipocytes.

Yiting Lei1, Meng Yang1, Xiaoyun Jiang1

  • 1Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, Institute of Aging Research, School of Medical Technology, Guangdong Medical University, Dongguan, China.

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|March 30, 2026
PubMed
Summary

Cellular senescence in white adipose tissue is linked to aging. We found that cytosolic phosphoenolpyruvate carboxykinase (Pck1) regulates mitochondrial function and inflammation, offering a potential target for age-related diseases.

Keywords:
Pck1TCA cycleagingcGAS/STING signalingcellular senescencewhite adipose tissue

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Area of Science:

  • Aging biology
  • Metabolic disorders
  • Cellular senescence

Background:

  • Cellular senescence in white adipose tissues (WAT) is an early aging sign, but mechanisms are unclear.
  • Understanding WAT senescence is crucial for addressing age-related metabolic dysfunction and inflammaging.

Purpose of the Study:

  • To identify key regulators of mitochondrial function and inflammaging in aging WAT.
  • To elucidate the role of cytosolic phosphoenolpyruvate carboxykinase (Pck1) in WAT senescence and metabolic health.

Main Methods:

  • Investigated Pck1 expression in aging gonadal and inguinal WAT.
  • Utilized adipocyte-specific Pck1 deficiency models.
  • Performed untargeted metabolomics and isotope-tracing analyses.
  • Examined the effects of fumarate supplementation and fumarate hydratase (Fh1) overexpression.

Main Results:

  • Pck1 expression decreased with age in WAT, and its deficiency accelerated inflammaging and metabolic disorders.
  • Pck1 loss impaired cataplerosis, leading to fumarate accumulation in adipocytes.
  • Fumarate accumulation disrupted mitochondrial homeostasis, increased oxidative stress, and activated the cGAS/STING pathway.
  • Fh1 overexpression reduced fumarate and attenuated adipocyte inflammaging.

Conclusions:

  • Pck1 is a critical regulator of mitochondrial metabolic homeostasis in WAT.
  • Pck1 deficiency promotes adipocyte inflammaging and metabolic dysfunction via fumarate accumulation and cGAS/STING activation.
  • Targeting Pck1 may offer a therapeutic strategy for age-related diseases.