Cholesterol-containing lipid crystals can directly stiffen the rat steatotic liver before fibrosis

Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by liver steatosis with cardiometabolic risk factors like dyslipidemia. Patients may progress from steatosis alone to complications such as fibrosis, end-stage liver disease, and hepatocellular carcinoma. The cause of progression is unclear. We previously showed that liver stiffening can drive fibrosis. However, the mechanical contributions of hepatic lipid and especially cholesterol accumulation are not known. We used rat dietary models to investigate how lipid accumulation affects liver mechanics. Liver stiffness was measured using rheology and magnetic resonance elastography, and associations between stiffness and lipid droplets (LDs) or cholesterol-containing lipid crystals were measured by microindentation-visualization. Polarized light, confocal reflection, and cryo-electron microscopy were employed to assess crystal abundance and structure. LDs and crystals extracted from livers were embedded in fibrous tissue mimics to isolate mechanical effects away from inflammation or fibrosis. Methyl-β-cyclodextrin perfusion was performed to assess whether cholesterol depletion reduced crystal abundance and tissue stiffness. Increased hepatic cholesterol storage led to the formation of cholesterol-containing lipid crystals in the liver. Steatotic livers with crystals stiffened before fibrosis while steatotic livers without crystals did not stiffen or fibrose. Lipid crystals stiffened tissue mimics while LDs did not, suggesting that crystals directly cause stiffening. Cholesterol depletion reduced crystal abundance and reverted tissue stiffness to near controls without changing inflammation, suggesting key roles for cholesterol in tissue stiffening. Lipid crystals cause profibrogenic liver stiffening, connecting high dietary cholesterol to MASLD progression, and may be a target for new diagnostic tools and therapeutics for progressive MASLD.

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Publication Details

Journal
Proceedings of the National Academy of Sciences
Published
2026-01-07
DOI
https://doi.org/10.1073/pnas.2518060123
Primary Topic
Liver Disease Diagnosis and Treatment
Type
article
Field-Weighted Citation Impact
0.00

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article

Cholesterol-containing lipid crystals can directly stiffen the rat steatotic liver before fibrosis

Abigail E. Loneker, Tatiana Kisseleva, Kandice R. Levental, Rebecca G. Wells et al.
Proceedings of the National Academy of Sciences
Liver Disease Diagnosis and Treatment
article

Cholesterol-containing lipid crystals can directly stiffen the rat steatotic liver before fibrosis

Abigail E. Loneker, Tatiana Kisseleva, Kandice R. Levental, Rebecca G. Wells, Elaine M. Mihelc, Yasmine Safraou, D. Li, Ingolf Sack, Sadatsugu Sakane, Jamie Ford, Paul A. Janmey, Ilya Levental
article en

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by liver steatosis with cardiometabolic risk factors like dyslipidemia. Patients may progress from steatosis alone to complications such as fibrosis, end-stage liver disease, and hepatocellular carcinoma. The cause of progression is unclear. We previously showed that liver stiffening can drive fibrosis. However, the mechanical contributions of hepatic lipid and especially cholesterol accumulation are not known. We used rat dietary models to investigate how lipid accumulation affects liver mechanics. Liver stiffness was measured using rheology and magnetic resonance elastography, and associations between stiffness and lipid droplets (LDs) or cholesterol-containing lipid crystals were measured by microindentation-visualization. Polarized light, confocal reflection, and cryo-electron microscopy were employed to assess crystal abundance and structure. LDs and crystals extracted from livers were embedded in fibrous tissue mimics to isolate mechanical effects away from inflammation or fibrosis. Methyl-β-cyclodextrin perfusion was performed to assess whether cholesterol depletion reduced crystal abundance and tissue stiffness. Increased hepatic cholesterol storage led to the formation of cholesterol-containing lipid crystals in the liver. Steatotic livers with crystals stiffened before fibrosis while steatotic livers without crystals did not stiffen or fibrose. Lipid crystals stiffened tissue mimics while LDs did not, suggesting that crystals directly cause stiffening. Cholesterol depletion reduced crystal abundance and reverted tissue stiffness to near controls without changing inflammation, suggesting key roles for cholesterol in tissue stiffening. Lipid crystals cause profibrogenic liver stiffening, connecting high dietary cholesterol to MASLD progression, and may be a target for new diagnostic tools and therapeutics for progressive MASLD.

Proceedings of the National Academy of SciencesVol. 123(2)
University of California San Diego (US), Humboldt-Universität zu Berlin (DE), And Technology Research (United Kingdom) (GB), Institute of Structural and Molecular Biology (GB), University of Virginia (US), Freie Universität Berlin (DE), Charité - Universitätsmedizin Berlin (DE), University of Pennsylvania (US)
National Science Foundation, American Liver Foundation, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Biomedical Imaging and Bioengineering, Division of Civil, Mechanical and Manufacturing Innovation
Good health and well-being
Openalex Percentile: Top 97%
Liver Disease Diagnosis and Treatment
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