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Inflammation and metabolic dysfunction: links to cardiovascular diseases
- Source :
- American Journal of Physiology-Heart and Circulatory Physiology. 302:H2148-H2165
- Publication Year :
- 2012
- Publisher :
- American Physiological Society, 2012.
-
Abstract
- Abdominal obesity is a major risk factor for cardiovascular disease, and recent studies highlight a key role of adipose tissue dysfunction, inflammation, and aberrant adipokine release in this process. An increased demand for lipid storage results in both hyperplasia and hypertrophy, finally leading to chronic inflammation, hypoxia, and a phenotypic change of the cellular components of adipose tissue, collectively leading to a substantially altered secretory output of adipose tissue. In this review we have assessed the adipo-vascular axis, and an overview of adipokines associated with cardiovascular disease is provided. This resulted in a first list of more than 30 adipokines. A deeper analysis only considered adipokines that have been reported to impact on inflammation and NF-κB activation in the vasculature. Out of these, the most prominent link to cardiovascular disease was found for leptin, TNF-α, adipocyte fatty acid-binding protein, interleukins, and several novel adipokines such as lipocalin-2 and pigment epithelium-derived factor. Future work will need to address the potential role of these molecules as biomarkers and/or drug targets.
- Subjects :
- medicine.medical_specialty
Physiology
Adipokine
Adipose tissue
Inflammation
Disease
Biology
Muscle hypertrophy
chemistry.chemical_compound
Adipokines
Metabolic Diseases
Physiology (medical)
Adipocyte
Internal medicine
medicine
Animals
Humans
Obesity
Abdominal obesity
Leptin
NF-kappa B
Rats
Endocrinology
Adipose Tissue
chemistry
Cardiovascular Diseases
Models, Animal
medicine.symptom
Cardiology and Cardiovascular Medicine
Subjects
Details
- ISSN :
- 15221539 and 03636135
- Volume :
- 302
- Database :
- OpenAIRE
- Journal :
- American Journal of Physiology-Heart and Circulatory Physiology
- Accession number :
- edsair.doi.dedup.....b6ab0a33b2afca1af9079af29e44c981