Adipose Tissue, Inflammation, and Cardiovascular Disease
Abstract
Mounting evidence highlights the role of adipose tissue in the development of a systemic inflammatory state that contributes to obesity-associated vasculopathy and cardiovascular risk. Circulating mediators of inflammation participate in the mechanisms of vascular insult and atheromatous change, and many of these inflammatory proteins are secreted directly from adipocytes and adipose tissue–derived macrophages. Several factors linking obesity with an increased cardiovascular risk have been identified. The adipocyte-specific secretory protein adiponectin is a particularly promising candidate in this context. Its levels are decreased in obesity. Adiponectin may mediate some of its demonstrated cardioprotective effects through its anti-inflammatory properties. In addition to decreased expression of beneficial adipokines, secretion of a host of inflammatory factors from visceral adipose tissue may contribute to the increased cardiovascular risk associated with obesity. The cardioprotective effects of many of the most popular drug regimens corroborate these conclusions, demonstrating that along with improvements in other therapeutic end points, they mediate improvements in systemic inflammation. In some cases, these improvements are attributable to direct suppression of inflammatory signaling in adipocytes. The targeted suppression of various proinflammatory cascades in adipocytes specifically represents an exciting new therapeutic opportunity for the cardiovascular disease area.
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Chronic systemic inflammation contributes to vascular injury and progression of atheromatous plaque.
“Chronic systemic inflammation contributes to vascular insult and atheromatous plaque progression.(16)”
From Endometriosis and Risk of Coronary Heart Disease (2016) · cites this paper as [16]
Obesity and inflammation are significantly related.
“considerable evidence suggests that obesity and inflammation are significantly related [163,486,575,581,642,647-664]”
In MESA, high intake of nuts and seeds (>=5 times/week) compared with low intake was associated with lower plasma CRP, IL-6 and fibrinogen.
“The MESA reported that a high intake of nuts and seeds ($5 times/week) compared with a low intake (rarely or no consumption) was associated with lower plasma concentrations of CRP, IL-6 and fibrinogen (367) .”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [367]
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- Authors
- Berg, A. H., & Scherer, P. E.
- Affiliations
- Brigham and Women's Hospital (US)
- Venue
- Circulation Research
- Published
- 2005-05-13
- Volume
- 96
- Issue
- 9
- Pages
- 939-949
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2133481218
- Cited by
- 2,113
- References
- 134
- Citations by year
- 2026: 30 · 2025: 70 · 2024: 48 · 2023: 63 · 2022: 86 · 2021: 106 · 2020: 103 · 2019: 79 · 2018: 83 · 2017: 114 · 2016: 140 · 2015: 121 · 2014: 153 · 2013: 154 · 2012: 126
- FWCI
- 13.68
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK 55758, R01DK055758)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- adipose tissue, systemic inflammation, obesity, cardiovascular risk, adiponectin, adipocytes, adipokines, atherosclerosis, vascular dysfunction, cardioprotection, anti-inflammatory therapy, pro-inflammatory signaling
- MeSH terms
- Adipose Tissue, Cardiovascular Diseases, Humans, Immunity, Innate, Inflammation, Insulin Resistance, Obesity, Weight Loss, Panniculitis, Cytokines, Metabolic Syndrome
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.
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