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Editorial
. 2013 Dec;62(6):1003-4.
doi: 10.1161/HYPERTENSIONAHA.113.01872. Epub 2013 Sep 23.

Cellular and molecular mechanisms of arterial stiffness associated with obesity

Jane A Leopold  1
Affiliations
Editorial

Cellular and molecular mechanisms of arterial stiffness associated with obesity

Jane A Leopold. Hypertension. 2013 Dec.
No abstract available

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Conflict of interest statement

Disclosures: NIH/NHLBI funding >$10,000

Figures

Figure 1
Figure 1
Cellular and molecular mechanisms of arterial stiffening. Arterial stiffening appears to be an active process that results from complementary and possibly co-dependent mechanisms involving the endothelium, vascular smooth muscle cells (SMC), and adventitial fibroblasts. Adipocytes, inflammatory cells, and T cells have also been implicated as mediators of arterial stiffening through paracrine mechanisms. Decreased bioavailable nitric oxide (•NO), increased oxidant stress and oxidative posttranslational modifications of proteins, endoplasmic reticulum (ER) stress, and mineralocorticoid receptor (MR) activation have all been implicated in the pathogenesis of increased vascular rigidity. There may also be evidence of extracellular matrix (ECM) remodeling with increased collagen deposition (wavy lines), decreased integrity of collagen or elastin, and decreased viscoelasticity of glycosaminoglycans (open circles). IEL, internal elastic lamina; EEL, external elastic lamina.
See this image and copyright information in PMC

Comment on

References

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