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CIDEC silencing attenuates diabetic nephropathy via inhibiting apoptosis and promoting autophagy

Gao-Shu Zheng1,2, Yan-Min Tan1, Yuan-Yuan Shang1

  • 1The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Cheeloo College of Medicine, Qilu Hospital, Shandong University, Jinan, Shandong, China.

Journal of Diabetes Investigation
|March 3, 2021
PubMed
Abstract

Insights

Cell death-inducing DFF45-like effector C (CIDEC) contributes to diabetic nephropathy (DN). Silencing CIDEC in rats improved insulin resistance, reduced kidney damage, and inhibited apoptosis, suggesting a therapeutic target for DN.

Area of Science:

  • Nephrology
  • Metabolic Diseases
  • Molecular Biology

Background:

  • Cell death-inducing DFF45-like effector C (CIDEC) is implicated in insulin resistance and diabetic nephropathy (DN) progression.
  • Understanding CIDEC's role in DN pathogenesis is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of CIDEC in the regulation of DN.
  • To elucidate the underlying mechanisms by which CIDEC influences DN progression.

Main Methods:

  • A type 2 diabetic rat model was established using a high-fat diet and streptozotocin.
  • Histopathological analysis, western blot, and gene silencing were employed to study CIDEC's effects.
  • The impact of CIDEC on high glucose-stimulated renal tubular epithelial cells was assessed.

Main Results:

  • Diabetic rats exhibited metabolic disturbances, kidney damage, increased apoptosis, and fibrosis.
  • CIDEC gene silencing ameliorated metabolic disorders, improved renal function, reduced apoptosis, and inhibited fibrosis.
  • In vitro, high glucose increased CIDEC expression, apoptosis, and decreased autophagy; CIDEC silencing reversed these effects.
  • Molecularly, CIDEC silencing reduced early growth response factor 1 (EGR1) and increased adipose triglyceride lipase (ATGL) expression.

Conclusions:

  • CIDEC gene silencing demonstrates a protective effect against DN progression.
  • Restoring autophagy and inhibiting apoptosis, potentially via EGR1 and ATGL modulation, are key mechanisms.
  • Targeting CIDEC presents a promising therapeutic strategy for managing diabetic nephropathy.
Keywords:
CIDECDiabetic nephropathy

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