Autophagy releases lipid that promotes fibrogenesis by activated hepatic stellate cells in mice and in human tissues
Open accessAbstract
Background & aims The pathogenesis of liver fibrosis involves activation of hepatic stellate cells, which is associated with depletion of intracellular lipid droplets. When hepatocytes undergo autophagy, intracellular lipids are degraded in lysosomes. We investigated whether autophagy also promotes loss of lipids in hepatic stellate cells to provide energy for their activation and extended these findings to other fibrogenic cells.Methods We analyzed hepatic stellate cells from C57BL/6 wild-type, Atg7(F/F), and Atg7(F/F)-GFAP-Cre mice, as well as the mouse stellate cell line JS1. Fibrosis was induced in mice using CCl(4) or thioacetamide (TAA); liver tissues and stellate cells were analyzed. Autophagy was blocked in fibrogenic cells from liver and other tissues using small interfering RNAs against Atg5 or Atg7 and chemical antagonists. Human pulmonary fibroblasts were isolated from samples of lung tissue from patients with idiopathic pulmonary fibrosis or from healthy donors.Results In mice, induction of liver injury with CCl(4) or TAA increased levels of autophagy. We also observed features of autophagy in activated stellate cells within injured human liver tissue. Loss of autophagic function in cultured mouse stellate cells and in mice following injury reduced fibrogenesis and matrix accumulation; this effect was partially overcome by providing oleic acid as an energy substrate. Autophagy also regulated expression of fibrogenic genes in embryonic, lung, and renal fibroblasts.Conclusions Autophagy of activated stellate cells is required for hepatic fibrogenesis in mice. Selective reduction of autophagic activity in fibrogenic cells in liver and other tissues might be used to treat patients with fibrotic diseases.
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HSC activation requires energy and relies on autophagy to release fatty acids through hydrolysis of retinyl esters, linked to endoplasmic reticulum stress.
“In addition to generation of intermediary metabolites through glycolysis, lipolysis, and glutaminolysis, the cells rely on activation of autophagy to release fatty acids through hydrolysis of retinyl esters (183) linked to endoplasmic reticulum stress (184).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [183]
Lipids released during autophagy provide an additional energy source for HSC activation, creating a possible antifibrotic target.
“Intracellular lipids released during autophagy act as an additional energy source for HSC activation, revealing another therapeutic vulnerability that could be targeted by antifibrotic strategies.122”
From An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH (2023) · cites this paper as [122]
In mouse models of liver fibrosis induced by thioacetamide or carbon tetrachloride, autophagy induction in hepatic stellate cells leads to lipid degradation and activates these cells to promote liver fibrosis.
“Interestingly, in mouse models of liver fibrosis induced by thioacetamide or carbon tetrachloride, the induction of autophagy in hepatic stellate cells led to lipid degradation and activated these cells to promote liver fibrosis110,111.”
From Autophagy in kidney homeostasis and disease (2020) · cites this paper as [110]
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Self-citation
- Authors
- Hernández–Gea, V., Ghiassi–Nejad, Z., Rozenfeld, R., Gordon, R., Fiel, M. I., Yue, Z., Czaja, M. J., & Friedman, S. L.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Albert Einstein College of Medicine (US)
- Corresponding author
- Friedman, Scott L.
- ORCID
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2012-04
- Volume
- 142
- Issue
- 4
- Pages
- 938-946
- ISSN
- 0016-5085 (ISSN-L)
- PMC
- PMC3439519
- OpenAlex
- W2005270729
- Cited by
- 654
- References
- 34
- Citations by year
- 2026: 38 · 2025: 38 · 2024: 40 · 2023: 52 · 2022: 45 · 2021: 67 · 2020: 58 · 2019: 42 · 2018: 46 · 2017: 54 · 2016: 52 · 2015: 49 · 2014: 42 · 2013: 24 · 2012: 7
- FWCI
- 24.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5T32GM007280, KO5AA018408, P20AA017067, R01 AA020709, R01DK044234, R01DK061498, R01NS060123, RO1DK56621)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Keywords
- autophagy, hepatic stellate cells, liver fibrosis, fibrogenesis, oleic acid, ATG7, ATG5, stellate cell activation, idiopathic pulmonary fibrosis, extracellular matrix accumulation, fibrotic diseases, thioacetamide, carbon tetrachloride
- MeSH terms
- Autophagy-Related Protein 5, Autophagy-Related Protein 7, Adenine, Adenosine Triphosphate, Animals, Autophagy, Carbon Tetrachloride, Cell Line, Energy Metabolism, Epoxy Compounds, Fibroblasts, Humans, Kidney, Liver, Liver Cirrhosis, Experimental, Lung, Mice, Inbred C57BL, Microtubule-Associated Proteins, Thioacetamide, Mice, Knockout, Oleic Acid, RNA Interference, Lipid Metabolism, Mice, Idiopathic Pulmonary Fibrosis, Hepatic Stellate Cells
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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