Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • RESEARCH HIGHLIGHT

Rebalancing cardiolipin biosynthesis to treat cardiomyopathy

By
  1. Alex Eccleston
Access through your institution
Buy or subscribe

Cardiomyopathies are often associated with mitochondrial dysfunction. Barth syndrome is a rare, potentially fatal congenital heart disease caused by defects in the mitochondrial enzyme Tafazzin (TAZ) and lacks effective therapies. In a recent Nature paper, Masud et al. performed genetic interaction screens and discovered an uncharacterized deacylase, ABHD18, that functions upstream of TAZ in the cardiolipin biosynthesis pathway. Inhibiting ABHD18 with a small molecule ameliorated TAZ mutant phenotypes in disease models.

Access options

Access through your institution

Rent or buy this article

Prices vary by article type

from$1.95

to$39.95

Learn more

Prices may be subject to local taxes which are calculated during checkout

doi: https://doi.org/10.1038/d41573-025-00161-4

References

  1. Masud, S. N. et al. Genetic suppression features ABHD18 as a Barth syndrome therapeutic target. Nature https://doi.org/10.1038/s41586-025-09373-5 (2025)

Download references

Nature Careers

Jobs

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing

Search

Advanced search

Quick links