How Do Elevated Triglycerides and Low HDL-Cholesterol Affect Inflammation and Atherothrombosis?
Open accessAbstract
This review article summarizes recent research into the mechanisms as to how elevated levels of triglyceride (TG) and low levels of high- density- lipoprotein cholesterol (HDL-C) contribute to inflammation and atherosclerosis. Evidence supports the role of TG-rich lipoproteins in signaling mechanisms via apolipoproteins C-III and free fatty acids leading to activation of NFKβ, VCAM-1 and other inflammatory mediators which lead to fatty streak formation and advanced atherosclerosis. Moreover, the cholesterol content in TG-rich lipoproteins has been shown to predict CAD risk better than LDL-C. In addition to reverse cholesterol transport, HDL has many other cardioprotective effects which include regulating immune function. The "functionality" of HDL appears more important than the level of HDL-C. Insulin resistance and central obesity underlie the pathophysiology of elevated TG and low HDL-C in metabolic syndrome and type 2 diabetes. Lifestyle recommendations including exercise and weight loss remain first line therapy in ameliorating insulin resistance and the adverse signaling processes from elevated levels of TG-rich lipoproteins and low HDL-C.
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TRLs have been implicated in pro-inflammatory signaling pathways, impairment of insulin sensitivity and upregulation of factors promoting thrombosis.
“Specifically, TRLs have been implicated in pro-inflammatory signaling pathways, impairment of insulin sensitivity and upregulation of factors promoting thrombosis.22,23”
From Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor?: New Insights From the Framingham Offspring Study (2016) · cites this paper as [22]
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- Authors
- Welty, F. K.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Welty, Francine K.
- ORCID
- Welty, Francine K.
- Venue
- Current Cardiology Reports
- Published
- 2013-07-24
- Volume
- 15
- Issue
- 9
- Pages
- 400-400
- ISSN
- 1523-3782 (ISSN-L)
- 1534-3170
- PMC
- PMC4465984
- OpenAlex
- W2020040555
- Cited by
- 221
- References
- 120
- Citations by year
- 2026: 16 · 2025: 23 · 2024: 26 · 2023: 34 · 2022: 21 · 2021: 23 · 2020: 16 · 2019: 19 · 2018: 15 · 2017: 12 · 2016: 7 · 2015: 3 · 2014: 4 · 2013: 2
- FWCI
- 0.94
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Current Cardiology Reports (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5p50hl083813-05)
- National Heart, Lung, and Blood Institute (P50-HL083813)
- National Institute of Dental and Craniofacial Research (R01DE018184)
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- triglyceride elevation, low HDL cholesterol, atherosclerosis, atherothrombosis, inflammation, triglyceride-rich lipoproteins, apolipoprotein C-III, free fatty acids, NF-κB, VCAM-1, fatty streak formation, coronary artery disease risk, reverse cholesterol transport, HDL function, immune function, insulin resistance, abdominal obesity, metabolic syndrome, type 2 diabetes, physical activity, weight loss
- MeSH terms
- Coronary Artery Disease, Humans, Inflammation, Cholesterol, HDL, Thrombosis, Triglycerides, Biomarkers, Inflammation Mediators, Metabolic Syndrome, Atherosclerosis, Plaque, Atherosclerotic
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