Targeting metabolically activated fibroblasts in the failing heart

Nikolaos G. Frangogiannis

doi:10.1038/s44161-024-00500-5

Targeting metabolically activated fibroblasts in the failing heart

Nikolaos G. Frangogiannis

Medicine

Research output: Contribution to journal › Comment/debate › peer-review

1 Scopus citations

Abstract

Myofibroblast activation requires nuclear translocation of ATP citrate lyase (ACLY) that triggers chromatin remodeling and the induction of fibrosis-associated genes. ACLY inhibition prevents myofibroblast conversion and causes de-differentiation of myofibroblasts to fibroblasts, indicating a potential therapeutic approach for heart failure.

Original language	English (US)
Pages (from-to)	782-784
Number of pages	3
Journal	Nature Cardiovascular Research
Volume	3
Issue number	7
DOIs	https://doi.org/10.1038/s44161-024-00500-5
State	Published - Jul 2024

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology (miscellaneous)
Cell Biology
Medicine (miscellaneous)
Cardiology and Cardiovascular Medicine

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10.1038/s44161-024-00500-5

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title = "Targeting metabolically activated fibroblasts in the failing heart",

abstract = "Myofibroblast activation requires nuclear translocation of ATP citrate lyase (ACLY) that triggers chromatin remodeling and the induction of fibrosis-associated genes. ACLY inhibition prevents myofibroblast conversion and causes de-differentiation of myofibroblasts to fibroblasts, indicating a potential therapeutic approach for heart failure.",

author = "Frangogiannis, {Nikolaos G.}",

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N2 - Myofibroblast activation requires nuclear translocation of ATP citrate lyase (ACLY) that triggers chromatin remodeling and the induction of fibrosis-associated genes. ACLY inhibition prevents myofibroblast conversion and causes de-differentiation of myofibroblasts to fibroblasts, indicating a potential therapeutic approach for heart failure.

AB - Myofibroblast activation requires nuclear translocation of ATP citrate lyase (ACLY) that triggers chromatin remodeling and the induction of fibrosis-associated genes. ACLY inhibition prevents myofibroblast conversion and causes de-differentiation of myofibroblasts to fibroblasts, indicating a potential therapeutic approach for heart failure.

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Targeting metabolically activated fibroblasts in the failing heart

Abstract

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