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Updated: Nov 10, 2025

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Reduced RECK levels accelerate skeletal muscle differentiation, improve muscle regeneration, and decrease fibrosis.

Jaime Gutiérrez1,2, David Gonzalez2, Rodrigo Escalona-Rivano1

  • 1Cellular Signaling and Differentiation Laboratory (CSDL), School of Medical Technology, Health Sciences Faculty, Universidad San Sebastian, Santiago, Chile.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|April 3, 2021
PubMed
Summary
This summary is machine-generated.

Reversion-inducing-cysteine-rich protein with kazal motifs (RECK) acts as a myogenic repressor, inhibiting skeletal muscle differentiation and regeneration. Reducing RECK levels accelerates muscle formation and diminishes fibrosis, suggesting RECK as a therapeutic target for muscle-wasting diseases.

Keywords:
MMPRECKmuscle fibrosisregenerationskeletal muscle differentiation

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Area of Science:

  • Muscle biology
  • Extracellular matrix dynamics
  • Cell signaling

Background:

  • Skeletal muscle regeneration relies on extracellular matrix (ECM) homeostasis, regulated by matrix-metalloproteinases (MMPs).
  • RECK (reversion-inducing-cysteine-rich protein with kazal motifs) is a known negative regulator of MMPs, but its role in muscle biology is unclear.

Purpose of the Study:

  • To investigate the function of RECK in skeletal muscle differentiation, regeneration, and fibrosis.
  • To elucidate RECK's impact on myogenic signaling pathways.

Main Methods:

  • Studied RECK expression during C2C12 myoblast differentiation and satellite cell activation.
  • Utilized RECK knockdown and overexpression in myoblasts.
  • Examined RECK's role in a mouse model of skeletal muscle regeneration and fibrosis (Reck± mice).

Main Results:

  • RECK is transiently upregulated during muscle differentiation and regeneration.
  • Reduced RECK accelerates myoblast differentiation and myotube formation, altering Notch-1, p38, and AKT signaling.
  • RECK deficiency (Reck±) accelerates muscle regeneration and significantly reduces fibrosis in a chronic muscle damage model.

Conclusions:

  • RECK functions as a myogenic repressor, inhibiting muscle formation and regeneration.
  • RECK modulation impacts key signaling pathways involved in myogenesis.
  • RECK represents a potential therapeutic target for treating muscle-wasting conditions and fibrosis.