KLF13 RESTRAINS DLL4-MUSCULAR NOTCH2 AXIS - TO IMPROVE SARCOPENIA

Sep 29, 2026

Krüppel-like factor 13 (KLF13) is highly expressed in skeletal muscle and regulates cellular energy metabolism, with suspected roles in sarcopenia. In a dexamethasone-induced muscle atrophy mouse model, KLF13 knockout reduced muscle strength, muscle weight, and exhaustive running distance. KLF13 overexpression preserved muscle mass and performance in vivo, while clofoctol protected against atrophy. Mechanistically, KLF13 suppresses Dll4, inhibiting the Dll4-Notch2 axis, and dexamethasone blocks KLF13 transcription and promotes KLF13 ubiquitination.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages1

Reading Time3 min

AccessFree to download

Abstract

Study models and phenotypes

Molecular mechanism: KLF13-Dll4-Notch2 axis

FAQs

What happens to muscle function when KLF13 is knocked out in the dexamethasone mouse model?

Compared with controls, the KLF13 knockout group shows decreased overall muscle strength, reduced muscle weight for major muscles, and a shorter exhaustive running distance.

How does KLF13 overexpression affect muscle atrophy in vivo?

KLF13 overexpression preserves muscle mass and improves exhaustive running distance in a diabetes-induced skeletal muscle atrophy model.

What mechanism links KLF13 to prevention of muscle atrophy?

Transcriptome and luciferase assays identify Dll4 as a target of KLF13; KLF13 suppresses Dll4 expression, inhibiting the Dll4-Notch2 axis and preventing atrophy.

Sep 29, 2026

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