Inhibition of ATP-citrate lyase improves NASH, liver fibrosis, and dyslipidemia
Open accessAbstract
Elevated liver de novo lipogenesis contributes to non-alcoholic steatohepatitis (NASH) and can be inhibited by targeting acetyl-CoA carboxylase (ACC). However, hypertriglyceridemia limits the use of pharmacological ACC inhibitors as a monotherapy. ATP-citrate lyase (ACLY) generates acetyl-CoA and oxaloacetate from citrate, but whether inhibition is effective for treating NASH is unknown. Here, we characterize a new mouse model that replicates many of the pathological and molecular drivers of NASH and find that genetically inhibiting ACLY in hepatocytes reduces liver malonyl-CoA, oxaloacetate, steatosis, and ballooning as well as blood glucose, triglycerides, and cholesterol. Pharmacological inhibition of ACLY mirrors genetic inhibition but has additional positive effects on hepatic stellate cells, liver inflammation, and fibrosis. Mendelian randomization of human variants that mimic reductions in ACLY also associate with lower circulating triglycerides and biomarkers of NASH. These data indicate that inhibiting liver ACLY may be an effective approach for treatment of NASH and dyslipidemia.
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ATP citrate lyase inhibition may reduce steatosis and fibrosis through direct inhibition of HSC activation.
“Similarly, pharmacological or genetic inhibition of ATP citrate lyase, which acts upstream of ACC1/2, reduces steatosis and fibrosis, possibly through direct inhibition of HSC activation (192).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [192]
Pharmacological or genetic inhibition of ATP citrate lyase reduces steatosis and fibrosis.
“Similarly, pharmacological or genetic inhibition of ATP citrate lyase, which acts upstream of ACC1/2, reduces steatosis and fibrosis, possibly through direct inhibition of HSC activation (192).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [192]
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- Authors
- Morrow, M. R., Batchuluun, B., Wu, J., Ahmadi, E., Leroux, J. M., Mohammadi-Shemirani, P., Desjardins, E. M., Wang, Z., Tsakiridis, E. E., Lavoie, D. C. T., Reihani, A., Smith, B. K., Kwiecien, J. M., Lally, J. S. V., Nero, T. L., Parker, M. W., Ask, K., Scott, J. W., Jiang, L., Paré, G., Pinkosky, S. L., & Steinberg, G. R.
- Affiliations
- McMaster University (CA)
- City Of Hope National Medical Center (US)
- St. Joseph’s Healthcare Hamilton (CA)
- The University of Melbourne (AU)
- Population Health Research Institute (CA)
- Esperion Therapeutics (United States) (US)
- Corresponding author
- Steinberg, Gregory R.
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2022-06
- Volume
- 34
- Issue
- 6
- Pages
- 919-936.e8
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W4281714255
- Cited by
- 199
- References
- 68
- Citations by year
- 2026: 50 · 2025: 46 · 2024: 55 · 2023: 39 · 2022: 9
- FWCI
- 26.89
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
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- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 371 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research (201709FDN-CEBA-116200)
- Novo Nordisk
- AstraZeneca
- Esperion Therapeutics
- Merck
- Diabetes Canada (DI-5-17-5302)
- McMaster University
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- ATP citrate lyase, nonalcoholic steatohepatitis, liver fibrosis, dyslipidemia, de novo lipogenesis, acetyl-CoA carboxylase, malonyl-CoA, oxaloacetate, hepatic steatosis, hepatic stellate cells, liver inflammation, hypertriglyceridemia, Mendelian randomization
- MeSH terms
- Acetyl-CoA Carboxylase, Animals, ATP Citrate (pro-S)-Lyase, Liver, Liver Cirrhosis, Oxaloacetates, Triglycerides, Dyslipidemias, Mice, Non-alcoholic Fatty Liver Disease
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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