Macrophage-specific PHGDH protects against MAFLD by suppressing TAK1
Open accessAbstract
Metabolic dysfunction-associated fatty liver disease (MAFLD) is a progressive disease with only one approved treatment currently available. Hepatic phosphoglycerate dehydrogenase (PHGDH), the rate-limiting enzyme of the serine biosynthesis pathway, regulates MAFLD development. However, the role of macrophage PHGDH in MAFLD progression remains unclear. Here, we demonstrate that the lipotoxicity inducer palmitic acid (PA) significantly increases macrophage PHGDH expression and that PHGDH deficiency in macrophages promotes PA-induced inflammatory responses. Myeloid-specific PHGDH deficiency exacerbates MAFLD in mice. Mechanistically, tetrameric PHGDH binds to transforming growth factor-β-activated kinase 1 (TAK1) to inhibit its interaction with TAK1 binding protein 1 (TAB1), sequentially suppressing the activation of TAK1 and downstream NF-κB and MAPK signaling. Inhibition of TAK1 activation slows the development of metabolic dysfunction-associated steatohepatitis (MASH) caused by myeloid PHGDH knockout. Importantly, adeno-associated virus-mediated PHGDH overexpression in liver macrophages alleviates MAFLD in mice. Collectively, these results identify macrophage PHGDH as a promising therapeutic agent for MAFLD.
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PHGDH is a novel target for metabolic immune precision therapy in MASLD.
“nominating PHGDH as a novel target for metabolic immune precision therapy in MASLD (64).”
From Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics (2026) · cites this paper as [64]
Myeloid-specific PHGDH deficiency exacerbates diet-induced steatohepatitis, whereas its overexpression confers protection.
“Myeloid specific PHGDH deficiency exacerbates diet induced steatohepatitis, whereas its overexpression confers protection, nominating PHGDH as a novel target for metabolic immune precision therapy in MASLD (64).”
From Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics (2026) · cites this paper as [64]
Under lipotoxic stress, tetrameric PHGDH directly binds and inhibits TAK1, thereby blocking the NF-κB/MAPK inflammatory cascade.
“Specifically, under lipotoxic stress, tetrameric PHGDH directly binds and inhibits transforming growth factor-β-activated kinase 1 (TAK1), thereby blocking the NF-κB/MAPK inflammatory cascade.”
From Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics (2026) · cites this paper as [64]
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- Authors
- Hu, P., Shan, X., Dong, H., Yu, S., Wang, B., Xiong, H., Ji, Z., Jing, W., Cui, Y., Li, Z., Zhou, Y., Wang, Z., Wang, J., Tang, J., Wang, T., Xie, K., & Yu, Q.
- Affiliations
- Tianjin Medical University General Hospital (CN)
- University of Electronic Science and Technology of China (CN)
- State Key Laboratory of Experimental Hematology (CN)
- Tianjin Medical University Cancer Institute and Hospital (CN)
- Tianjin Medical University (CN)
- Corresponding author
- Xie, Keliang
- Yu, Qiujing
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2025-03
- Volume
- 44
- Issue
- 3
- Pages
- 115426
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W4408495125
- Semantic Scholar
- 15d06e010cce0614b8deeba6652f288ec15ac4f6
- Cited by
- 12
- References
- 61
- Citations by year
- 2026: 6 · 2025: 6
- FWCI
- 8.25
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (82300682, 32471218, 82273088, 82350116, 82402504)
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Keywords
- non-alcoholic fatty liver disease, serine biosynthesis, TAK1, TAB1, palmitic acid, lipotoxicity, myeloid-specific knockout, NF-κB signaling, MAPK signaling, nonalcoholic steatohepatitis, hepatic macrophages, AAV gene therapy, inflammation
- MeSH terms
- MAP Kinase Kinase Kinase 7, Animals, Fatty Liver, Humans, Liver, Macrophages, Male, Mice, Inbred C57BL, NF-kappa B, Mice, Knockout, Palmitic Acid, MAP Kinase Kinase Kinases, Phosphoglycerate Dehydrogenase, Mice
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