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Review
. 2022 Feb 18:13:842636.
doi: 10.3389/fphar.2022.842636. eCollection 2022.

Platelets in Non-alcoholic Fatty Liver Disease

Affiliations
Review

Platelets in Non-alcoholic Fatty Liver Disease

Andrea Dalbeni et al. Front Pharmacol. .

Abstract

Non alcoholic steatohepatitis (NASH) is the inflammatory reaction of the liver to excessive accumulation of lipids in the hepatocytes. NASH can progress to cirrhosis and hepatocellular carcinoma (HCC). Fatty liver is the hepatic manifestation of metabolic syndrome. A subclinical inflammatory state is present in patients with metabolic alterations like insulin resistance, type-2 diabetes, obesity, hyperlipidemia, and hypertension. Platelets participate in immune cells recruitment and cytokines-induced liver damage. It is hypothesized that lipid toxicity cause accumulation of platelets in the liver, platelet adhesion and activation, which primes the immunoinflammatory reaction and activation of stellate cells. Recent data suggest that antiplatelet drugs may interrupt this cascade and prevent/improve NASH. They may also improve some metabolic alterations. The pathophysiology of inflammatory liver disease and the implication of platelets are discussed in details.

Keywords: Kupffer cells; antiplatelet agents; fibrosis; hepatic stellate cells; inflammation; non-alcoholic fatty liver disease; non-alcoholic steatohepatitis; platelets.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The handling editor declared a past co-authorship with one of the authors PM.

Figures

FIGURE 1
FIGURE 1
Main determinants of NAFLD/NASH

References

    1. Abdel-Moneim A., Mahmoud B., Sultan E. A., Mahmoud R. (2019). Relationship of Leukocytes, Platelet Indices and Adipocytokines in Metabolic Syndrome Patients. Diabetes Metab. Syndr. 13 (1), 874–880. 10.1016/J.DSX.2018.12.016 - DOI - PubMed
    1. Adori C., Daraio T., Kuiper R., Barde S., Horvathova L., Yoshitake T., et al. (2021). Disorganization and Degeneration of Liver Sympathetic Innervations in Nonalcoholic Fatty Liver Disease Revealed by 3D Imaging. Sci. Adv. 7 (30), eabg5733. 10.1126/SCIADV.ABG5733 - DOI - PMC - PubMed
    1. Akkerman J. W. N. (2008). From Low-Density Lipoprotein to Platelet Activation. Int. J. Biochem. Cel Biol. 40 (11), 2374–2378. 10.1016/J.BIOCEL.2008.04.002 - DOI - PubMed
    1. Alexander M., Loomis A. K., Van Der Lei J., Duarte-Salles T., Prieto-Alhambra D., Ansell D., et al. (2019). Non-alcoholic Fatty Liver Disease and Risk of Incident Acute Myocardial Infarction and Stroke: Findings from Matched Cohort Study of 18 Million European Adults. BMJ 367, l5367. 10.1136/BMJ.L5367 - DOI - PMC - PubMed
    1. Amarapurkar D. N., Hashimoto E., Lesmana L. A., Sollano J. D., Chen P. J., Goh K. L. (2007). How Common Is Non-alcoholic Fatty Liver Disease in the Asia-Pacific Region and Are There Local Differences? J. Gastroenterol. Hepatol. 22 (6), 788–793. 10.1111/J.1440-1746.2007.05042.X - DOI - PubMed

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