Bharadwaj A, Taneja M, Dubey S, Saxena A. Very low-density lipoprotein and the human health. World J Exp Med 2026; 16(1): 117024 [DOI: 10.5493/wjem.v16.i1.117024]
Corresponding Author of This Article
Alok Bharadwaj, PhD, Associate Professor, Department of Biotechnology, GLA University, 17 Kilometre Mile Stone, Mathura-Delhi Highway NH-1, Mathura 281406, Uttar Pradesh, India. alok.bhardwaj@gla.ac.in
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Biochemical Research Methods
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Review
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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/
Mar 20, 2026 (publication date) through Mar 20, 2026
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World Journal of Experimental Medicine
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2220-315x
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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Bharadwaj A, Taneja M, Dubey S, Saxena A. Very low-density lipoprotein and the human health. World J Exp Med 2026; 16(1): 117024 [DOI: 10.5493/wjem.v16.i1.117024]
Alok Bharadwaj, Manas Taneja, Sneha Dubey, Department of Biotechnology, GLA University, Mathura 281406, Uttar Pradesh, India
Aditya Saxena, Department of Bioinformatics, Faculty of Engineering & Technology, Marwadi University, Rajkot 360003, Gujarāt, India
Author contributions: Bharadwaj A contributed to conceptualization, writing original draft; Taneja M and Saxena A contributed to final editing, improvisation; Dubey S contributed to interpretation; Dubey S and Saxena A contributed to analysis and review the manuscript; Saxena A contributed to typesetting.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Alok Bharadwaj, PhD, Associate Professor, Department of Biotechnology, GLA University, 17 Kilometre Mile Stone, Mathura-Delhi Highway NH-1, Mathura 281406, Uttar Pradesh, India. alok.bhardwaj@gla.ac.in
Received: November 27, 2025 Revised: December 23, 2025 Accepted: February 12, 2026 Published online: March 20, 2026 Processing time: 108 Days and 21.2 Hours
Abstract
Very low-density lipoprotein (VLDL), released in the liver, is the only lipoprotein that includes apolipoprotein B (marker for cardiovascular risk), triglycerides, and cholesterol. VLDL is essential in transporting lipids and cholesterol to organs and cells for utilization. VLDL also contributes significantly to the advancement of atherosclerotic heart disease. We comprehensively summarize VLDL’s physiological roles and data supporting its pathological effects. VLDL has been proven to promote atherosclerosis in the metabolic syndrome. VLDL isolated from metabolic syndrome patients is cytotoxic to atrial myocytes, causing atrial myopathy and contributing to atrial fibrillation. Several endocrine diseases may impact VLDL levels, which can be boosted by supplementing with progesterone, estrogen, cortisol, and growth hormones. VLDL stimulates high blood pressure by secreting aldosterone. VLDL induces neuroinflammation, which may lead to cognitive impairment. VLDL is linked to chronic renal illness, autoimmune disorders, and some skin diseases. VLDL production outside the liver caused by intestinal dysbiosis is considered harmful. New evidence reveals that VLDL metabolism has a role in the development and risk of cancer, as well as sleep disturbances. Aside from this, VLDL metabolism and carcinogenesis might be altered by the VLDL receptor. Overall, growing findings point to the role of VLDL in many illnesses.
Core Tip: The liver secretes very low-density lipoprotein (VLDL), implicated in diseases such as atherosclerosis, metabolic-associated fatty liver disease, cognitive impairment, metabolic syndrome, autoimmune disorders, breast cancer, and head and neck cancer. VLDL contributes to atrial myopathy in the preclinical stage of atrial fibrillation and exhibits cytotoxic effects in myocardial infarction, though the mechanism remains unclear. Endocrine disorders can alter VLDL levels, and VLDL has been shown to increase aldosterone production. Its pathogenic role extends to extrahepatic release, neurological disorders, sleep disturbances, and various malignancies. Understanding VLDL regulation and metabolism, rather than just its levels, may clarify its role in disease and guide targeted therapeutic strategies.
