Cardiomyopathy with lethal arrhythmias associated with inactivation of KLHL24

Hum Mol Genet. 2019 Jun 1;28(11):1919-1929. doi: 10.1093/hmg/ddz032.

Abstract

Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiovascular disorder, yet the genetic cause of up to 50% of cases remains unknown. Here, we show that mutations in KLHL24 cause HCM in humans. Using genome-wide linkage analysis and exome sequencing, we identified homozygous mutations in KLHL24 in two consanguineous families with HCM. Of the 11 young affected adults identified, 3 died suddenly and 1 had a cardiac transplant due to heart failure. KLHL24 is a member of the Kelch-like protein family, which acts as substrate-specific adaptors to Cullin E3 ubiquitin ligases. Endomyocardial and skeletal muscle biopsies from affected individuals of both families demonstrated characteristic alterations, including accumulation of desmin intermediate filaments. Knock-down of the zebrafish homologue klhl24a results in heart defects similar to that described for other HCM-linked genes providing additional support for KLHL24 as a HCM-associated gene. Our findings reveal a crucial role for KLHL24 in cardiac development and function.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Animals
  • Arrhythmias, Cardiac / genetics*
  • Arrhythmias, Cardiac / mortality
  • Arrhythmias, Cardiac / physiopathology
  • Cardiomyopathy, Hypertrophic / genetics
  • Cardiomyopathy, Hypertrophic / mortality*
  • Cardiomyopathy, Hypertrophic / pathology
  • Death, Sudden, Cardiac / pathology
  • Desmin / genetics
  • Disease Models, Animal
  • Female
  • Genetic Linkage / genetics
  • Heart Failure / genetics*
  • Heart Failure / mortality
  • Heart Failure / physiopathology
  • Homozygote
  • Humans
  • Male
  • Mutation
  • Pedigree
  • Phenotype
  • Repressor Proteins / genetics*
  • Zebrafish / genetics

Substances

  • Desmin
  • KLHL24 protein, human
  • Repressor Proteins