Myocardial infarction accelerates the progression of MASH by triggering immunoinflammatory response and induction of periostin
Open accessAbstract
Patients with metabolic dysfunction-associated steatotic liver disease (MASLD), especially advanced metabolic dysfunction-associated steatohepatitis (MASH), have an increased risk of cardiovascular diseases (CVDs). Whether CVD events will, in turn, influence the pathogenesis of MASLD remains unknown. Here, we show that myocardial infarction (MI) accelerates hepatic pathological progression of MASLD. Patients with MASLD who experience CVD events after their diagnosis exhibit accelerated liver fibrosis progression. MI promotes hepatic fibrosis in mice with MASH, accompanied by elevated circulating Ly6C hi monocytes and their recruitment to damaged liver tissues. These adverse effects are significantly abrogated when deleting these cells. Meanwhile, MI substantially increases circulating and cardiac periostin levels, which act on hepatocytes and stellate cells to promote hepatic lipid accumulation and fibrosis, finally exacerbating hepatic pathological progression of MASH. These preclinical and clinical results demonstrate that MI alters systemic homeostasis and upregulates pro-fibrotic factor production, triggering cross-disease communication that accelerates hepatic pathological progression of MASLD.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The results extend current MASLD frameworks into an integrated mechanical-metabolic-inflammatory axis.
“our results extend current MASLD frameworks, traditionally centered on metabolic dysregulation and inflammation, into an integrated mechanical–metabolic–inflammatory axis [44, 45, 46, 47, 48]”
From Liver Stiffness Rises Early in MASLD and Drives Inflammation, Lipid Dysmetabolism, and Fibrosis via Piezo1–YAP Mechanotransduction (2026) · cites this paper as [46]
Cites
Heart Disease and Stroke Statistics—2023 Update: A Report From the American Heart Association
Tsao, C. W., Aday, A. W., Almarzooq, Z. I., Anderson, C. A. M., Arora, P., Avery, C. L., Baker-Smith, C. M., Beaton, A. Z., Boehme, A. K., Buxton, A. E., et al. (2023) · Circulation · doi:10.1161/cir.0000000000001123 · Cited by 8,300 · see citing works
Mechanisms of Fibrosis Development in Nonalcoholic Steatohepatitis
Schwabe, R. F., Tabas, I., & Pajvani, U. B. (2020) · Gastroenterology · doi:10.1053/j.gastro.2019.11.311 · Cited by 671 · see citing works
Tsuchida, T., Lee, Y. A., Fujiwara, N., Ybanez, M., Allen, B., Martins, S., Fiel, M. I., Goossens, N., Chou, H.-I., Hoshida, Y., et al. (2018) · Journal of Hepatology · doi:10.1016/j.jhep.2018.03.011 · Cited by 583 · see citing works
NAFLD as a driver of chronic kidney disease
Byrne, C. D., & Targher, G. (2020) · Journal of Hepatology · doi:10.1016/j.jhep.2020.01.013 · Cited by 449 · see citing works
Exercise plasma boosts memory and dampens brain inflammation via clusterin
De Miguel, Z., Khoury, N., Betley, M. J., Lehallier, B., Willoughby, D., Olsson, N., Yang, A. C., Hahn, O., Lu, N., Vest, R. T., et al. (2021) · Nature · doi:10.1038/s41586-021-04183-x · Cited by 422 · see citing works
Daemen, S., Gainullina, A., Kalugotla, G., He, L., Chan, M. M., Beals, J. W., Liss, K. H., Klein, S., Feldstein, A. E., Finck, B. N., et al. (2021) · Cell Reports · doi:10.1016/j.celrep.2020.108626 · Cited by 378 · see citing works
An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH
Tacke, F., Puengel, T., Loomba, R., & Friedman, S. L. (2023) · Journal of Hepatology · doi:10.1016/j.jhep.2023.03.038 · Cited by 321 · see citing works
Mózes, F. E., Lee, J. A., Vali, Y., Alzoubi, O., Staufer, K., Trauner, M., Paternostro, R., Stauber, R. E., Holleboom, A. G., van Dijk, A.-M., et al. (2023) · The Lancet Gastroenterology & Hepatology · doi:10.1016/s2468-1253(23)00141-3 · Cited by 214 · see citing works
Self-citationLoft, A., Alfaro, A. J., Schmidt, S. F., Pedersen, F. B., Terkelsen, M. K., Puglia, M., Chow, K. K., Feuchtinger, A., Troullinaki, M., Maida, A., et al. (2021) · Cell Metabolism · doi:10.1016/j.cmet.2021.06.005 · Cited by 129 · see citing works
Neuregulin 4 suppresses NASH-HCC development by restraining tumor-prone liver microenvironment
Zhang, P., Chen, Z., Kuang, H., Liu, T., Zhu, J., Zhou, L., Wang, Q., Xiong, X., Meng, Z., Qiu, X., et al. (2022) · Cell Metabolism · doi:10.1016/j.cmet.2022.07.010 · Cited by 105 · see citing works
Self-citation
Flagged first, then by citations
Cited by
Sorted by citations
Ma, J., Xie, N., Wang, Z., Liang, X., Han, Y., Zhao, Q., Wang, M., Lu, H., Kou, W., Alazawi, W., et al. (2026) · Advanced Science · doi:10.1002/advs.202519109 · Cited by 14 · see citing works
- Authors
- Xie, W., Gan, J., Zhou, X., Tian, H., Pan, X., Liu, W., Li, X., Du, J., Xu, A., Zheng, M., Wu, F., Li, Y., & Lin, Z.
- Affiliations
- Guangdong Medical College (CN)
- First Affiliated Hospital of Wenzhou Medical University (CN)
- Wenzhou Medical University (CN)
- Capital Medical University (CN)
- University of Hong Kong (HK)
- Corresponding author
- Wu, Fan
- Li, Yulin
- Lin, Zhuofeng
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2024-06
- Volume
- 36
- Issue
- 6
- Pages
- 1269-1286.e9
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W4399352323
- Cited by
- 55
- References
- 10
- Citations by year
- 2026: 25 · 2025: 25 · 2024: 5
- FWCI
- 16.78
- Type
- journal article
- Language
- en
- Update notices
- erratum (2024-07-02)
- 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, 368 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
- National Key Research and Development Program of China (2020YFA0803801)
- China National Funds for Distinguished Young Scientists (81925004)
- National Natural Science Foundation of China
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- myocardial infarction, non-alcoholic fatty liver disease, periostin, monocytes, immune-inflammatory response, liver fibrosis, hepatic lipid accumulation, hepatic stellate cells, cardiomyopathy
- MeSH terms
- Animals, Female, Humans, Inflammation, Liver, Liver Cirrhosis, Male, Mice, Inbred C57BL, Middle Aged, Monocytes, Myocardial Infarction, Cell Adhesion Molecules, Disease Progression, Hepatocytes, Mice
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 ›
Are you an author, or do you see a problem with this page? Request a review
