Clinical Outcome in KLHL24 Cardiomyopathy

Mathilde C S C Vermeer*, Karla F Arevalo Gomez, Martijn F Hoes, Jasper Tromp, Job A J Verdonschot, Michiel T H M Henkens, Herman H W Silljé, Maria C Bolling, Peter van der Meer*

*Corresponding author for this work

Research output: Contribution to journalComment/Letter to the editorAcademicpeer-review

Abstract

Pathogenic variants in Kelch-like family member 24 ( as a new cause for skin fragility KLHL24; NM_017644.3) were recently identified and cardiomyopathy. KLHL24 is part of a ubiquitin-ligase complex and mediates substrate recognition of intermediate filaments for proteasomal degradation (ie, keratins,1,2 vimentin,2 and desmin3,4). Several studies have shown that patients with heterozygous gain-of-function variants (HET-GOF), typically born with epidermolysis bullosa simplex,1,2 can develop dilated cardiomyopathy (DCM) with desmin-deficiency.3 Meanwhile, hypertrophic cardiomyopathy (HCM) with desmin-overload has been determined in patients with homozygous loss-of-function variants (HOM-LOF).4 This meta-analysis aims to summarize the findings of previous patient studies to determine the clinical outcome in KLHL24 cardiomyopathy.

Original languageEnglish
Pages (from-to)401-403
Number of pages3
JournalCirculation: Genomic and Precision Medicine
Volume16
Issue number4
DOIs
Publication statusPublished - 16 May 2023

Keywords

  • cardiomyopathy
  • desmin
  • dilated
  • heart failure
  • hypertrophic
  • Humans
  • Cardiomyopathies/genetics
  • Cardiomyopathy, Dilated

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