Aberrant iron distribution via hepatocyte-stellate cell axis drives liver lipogenesis and fibrosis
Open accessAbstract
Hepatocytes have important roles in liver iron homeostasis, abnormalities in which are tightly associated with liver steatosis and fibrosis. Here, we show that non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) are characterized by iron-deficient hepatocytes and iron overload in hepatic stellate cells (HSCs). Iron deficiency enhances hepatocyte lipogenesis and insulin resistance through HIF2α-ATF4 signaling. Elevated secretion of iron-containing hepatocyte extracellular vesicles (EVs), which are normally cleared by Kupffer cells, accounts for hepatocyte iron deficiency and HSC iron overload in NAFLD/NASH livers. Iron accumulation results in overproduction of reactive oxygen species that promote HSC fibrogenic activation. Conversely, blocking hepatocyte EV secretion or depleting EV iron cargo restores liver iron homeostasis, concomitant with mitigation of NAFLD/NASH-associated liver steatosis and fibrosis. Taken together, these studies show that iron distribution disorders contribute to the development of liver metabolic diseases.
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Monocyte-derived macrophages replace Kupffer cells that normally clear iron, causing iron overload, oxidative stress, and activation of HSCs into myofibroblasts.
“Second, monocyte-derived macrophages replace liver resident Kupffer cells that normally clear iron, resulting in iron overload, oxidative stress, and activation of HSCs into myofibroblasts (70, 74-77).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [74]
Iron shuttled by extracellular vesicles from hepatocytes to HSCs in MASH stimulates fibrogenesis through iron overload and oxidative stress, exacerbated by TGFβ-mediated suppression of cytoglobin.
“Iron can be shuttled by extracellular vesicles from hepatocytes to HSCs in MASH, stimulating fibrogenesis through iron overload and oxidative stress, an effect that is further exacerbated by TGFβ-mediated suppression of the antioxidant protein cytoglobin (CYGB) (74) (149).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [74]
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- Authors
- Gao, H., Jin, Z., Bandyopadhyay, G., Wang, G., Zhang, D., Rocha, K. C. E., Liu, X., Zhao, H., Kisseleva, T., Brenner, D. A., Karin, M., & Ying, W.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Gao, Hong
- Karin, Michael
- Ying, Wei
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2022-08
- Volume
- 34
- Issue
- 8
- Pages
- 1201-1213.e5
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC9365100
- OpenAlex
- W4289527021
- Cited by
- 224
- References
- 61
- Citations by year
- 2026: 46 · 2025: 84 · 2024: 55 · 2023: 31 · 2022: 8
- FWCI
- 32.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 366 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)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- National Institutes of Health (S10 OD026929)
- National Institute of Neurological Disorders and Stroke (P30 DK063491, P30 NS047101, P42ES010337, P50AA011999, R00DK115998, R01CA234128, R01DK099205, R01DK101737, R01DK11866, R01DK120714, R01DK125560, U01AA022614)
- University of California, San Diego
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- liver fibrosis, non-alcoholic fatty liver disease, steatohepatitis, hepatic stellate cells, extracellular vesicles, insulin resistance, reactive oxygen species, Kupffer cells, hepatic steatosis
- MeSH terms
- Animals, Disease Models, Animal, Fibrosis, Iron, Kupffer Cells, Liver, Liver Cirrhosis, Iron Overload, Hepatocytes, Lipogenesis, Hepatic Stellate Cells, Non-alcoholic Fatty Liver Disease
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