Eid N. Letter to the Editor: Microplastics as promoters of metabolic dysfunction-associated steatotic liver disease: Mechanistic insights and implications. World J Hepatol 2026; 18(6): 118615 [DOI: 10.4254/wjh.118615]
Corresponding Author of This Article
Nabil Eid, Associate Professor, MD, PhD, Department of Human Biology, School of Medicine, IMU University, Bukit Jalil, Kuala Lumpur 57000, Malaysia. nabilsaleheid@imu.edu.my
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
letter
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Share the Article
Eid N. Letter to the Editor: Microplastics as promoters of metabolic dysfunction-associated steatotic liver disease: Mechanistic insights and implications. World J Hepatol 2026; 18(6): 118615 [DOI: 10.4254/wjh.118615]
World J Hepatol. Jun 27, 2026; 18(6): 118615 Published online Jun 27, 2026. doi: 10.4254/wjh.118615
Letter to the Editor: Microplastics as promoters of metabolic dysfunction-associated steatotic liver disease: Mechanistic insights and implications
Nabil Eid
Nabil Eid, Department of Human Biology, School of Medicine, IMU University, Kuala Lumpur 57000, Malaysia
Author contributions: Eid N wrote, edited, and approved the final draft of the manuscript.
Conflict-of-interest statement: The author reports no relevant conflicts of interest for this article.
Corresponding author: Nabil Eid, Associate Professor, MD, PhD, Department of Human Biology, School of Medicine, IMU University, Bukit Jalil, Kuala Lumpur 57000, Malaysia. nabilsaleheid@imu.edu.my
Received: January 7, 2026 Revised: January 28, 2026 Accepted: March 6, 2026 Published online: June 27, 2026 Processing time: 164 Days and 4.7 Hours
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease worldwide and carries a substantial risk of progression to hepatocellular carcinoma. The detection of microplastics (MPs) in human tissues - including the brain, lung, liver, and blood - has emerged as an important environmental health concern. A recent study comprehensively summarized the potential mechanisms by which MPs may induce and exacerbate MASLD. The evidence discussed was largely derived from in vitro and preclinical studies and included hepatic lipid dysregulation, oxidative and endoplasmic reticulum stress, mitochondrial dysfunction, inflammatory signaling, fibrogenesis, gut dysbiosis, and endocrine disruption. This article comments on the study by Rajak et al, published in the recent issue of the World Journal of Hepatology, and specifically highlights how MPs-induced autophagy dysfunction may contribute to MASLD progression and its potential clinical implications.
Core Tip: Metabolic dysfunction-associated steatotic liver disease is the most prevalent chronic liver disease worldwide and carries a risk of progression to hepatocellular carcinoma. Microplastics have emerged as environmental hazards and have been detected in human tissues, including the liver, brain, and blood. Recent preclinical evidence links microplastic exposure to metabolic dysfunction-associated steatotic liver disease through mechanisms involving metabolic stress, inflammation, and autophagy dysfunction, with potential clinical implications.
