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Updated: Dec 29, 2025

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
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Regulated in Development and DNA Damage Responses 1 Prevents Dermal Adipocyte Differentiation and Is Required for

Guillermo C Rivera-Gonzalez1, Anna Klopot2, Kaitlyn Sabin3

  • 1Department of Molecular, Cellular and Developmental Biology and Department of Dermatology, Yale University, New Haven, Connecticut, USA; Current address: Department of Developmental Biology, Washington University School of Medicine in St. Louis, St. Louis, Missouri, USA.

The Journal of Investigative Dermatology
|February 8, 2020
PubMed

Insights

Regulated in DNA damage responses 1 (REDD1) normally limits skin fat cell growth. Loss of REDD1 causes dermal white adipose tissue (dWAT) expansion through increased fat cell size and number.

Area of Science:

  • Cell biology
  • Adipose tissue biology
  • Dermatology

Background:

  • Dermal white adipose tissue (dWAT) plays roles in skin homeostasis and disease.
  • The mTOR/protein kinase B pathway regulates adipogenesis, but the role of its inhibitor, REDD1, is unclear.

Purpose of the Study:

  • To investigate the role of REDD1 in regulating dermal white adipose tissue expansion.

Main Methods:

  • Mice lacking REDD1 were analyzed for adipose tissue characteristics.
  • In vitro studies assessed adipocyte precursor cell differentiation and lipid accumulation.

Main Results:

  • REDD1 knockout mice showed reduced body mass but expanded dWAT with increased adipocyte size and number.
  • Skin-derived adipocyte precursor cells from REDD1 knockouts exhibited enhanced differentiation.
  • Overexpression of REDD1 in 3T3L1 cells reduced differentiation sensitivity.

Conclusions:

  • REDD1 deficiency leads to dWAT expansion via hypertrophy and hyperplasia.
  • REDD1-dependent adipogenesis regulation offers potential therapeutic targets for skin-associated adipose tissue.

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