Periadventitial Adipose Tissue Plays a Critical Role in Vascular Remodeling

Takaoka, Minoru; Nagata, Daisuke; Kihara, Shinji; Shimomura, Iichiro; Kimura, Yu; Tabata, Yasuhiko; Saito, Yoshihiko; Nagai, Ryozo; Sata, Masataka

doi:10.1161/circresaha.109.199653

Cited by 184 publications

(188 citation statements)

References 43 publications

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“…D-47 is a novel drug which selectively lowers serum Lp(a) levels. Vascular injury model is a useful tools for investigating the mechanism of vascular remodeling because they invoke leukocyte adhesion and infiltration, proliferation of smooth muscle cells and neointima formation (9,10). Using this model and the double transgenic mice, we have shown that D-47 lowered serum levels of Lp(a) and possibly reduced vascular inflammation and neointima formation after vascular injury.…”

Section: Discussionmentioning

confidence: 95%

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A novel lipoprotein (a) lowering drug, D-47, decreases neointima thickening after vascular injury

et al. 2017

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: Although Lp(a) have been thought to be a cardiovascular risk factor, it is unclear whether lowering Lp(a) levels reduces the risk of cardiovascular diseases. No pharmacological agents which selectively reduce serum Lp(a) levels, and Lp(a) is present in primate but absent in common laboratory animals such as mice and pigs. In the present study we used transgenic mice of human Lp(a) and tested effect a novel Lp(a) lowering drug D-47 on neointima formation after vascular injury. D-47 successfully decreased plasma levels of Lp(a) and possibly inhibited neointima formation in Lp(a) transgenic mice. The results indicate that we can modulate plasma Lp(a) levels by pharmacologic agents and inhibit atherogenic properties of Lp(a) by reducing plasma levels of Lp(a).

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Section: Discussionmentioning

confidence: 95%

“…Vascular injury was induced in mice as described previously (9,10). A straight spring wire (0.38 mm in diameter, No.C -SF-15 -15, COOK) was inserted into the femoral artery and left in place for 1 minute to denude and dilate the artery.…”

Section: Production Of Vascular Injurymentioning

confidence: 99%

A novel lipoprotein (a) lowering drug, D-47, decreases neointima thickening after vascular injury

et al. 2017

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“…As indicated above, the expansion of adipose tissue seen in obesity is associated with adipose tissue inflammation, leading to an imbalanced secretion including (i) an enhanced release of pro-inflammatory adipokines, and (ii) a decreased release of anti-inflammatory adipokines (Table 3) as well as (iii) a dysbalance in contractile and relaxing factors released from PAAT (Table 4). Such a yin-and-yang pattern of cell secretion requires research aiming at (i) the inhibition of secretion and/or receptor sensitivity of pro-inflammatory and vasocontractile adipose-derived mediators, and (ii) the stimulation of secretion and/or receptor sensitivity of anti-inflammatory and vasorelaxing adipose-derived mediators (1,3,(31)(32)(33). It is noteworthy that the removal of PAAT enhances neointima formation after injury, which is attenuated by transplantation of subcutaneous adipose tissue (33).…”

Section: Pericardiummentioning

confidence: 99%

Adipoparacrinology: an Emerging Field in Biomedical Research

Chaldakov¹,

Tunçel²,

Bełtowski³

et al. 2012

Balkan Med J

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“…These fats are called "ectopic" fats. In particular, ectopic adipose tissue deposits have been found around the heart, coronary artery, and other arteries in human and animal models (16)(17)(18)(19)(20). The absence of adipose tissue around the aorta may promote the development of atherosclerosis.…”

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confidence: 99%

“…The absence of adipose tissue around the aorta may promote the development of atherosclerosis. Additionally, the presence of dysfunctional adipose tissue, exhibiting insulin resistance, around the aorta may also result in the development of atherosclerosis via the secretion of pro-insulin-resistant adipocytokines, such as monocyte chemoattractant protein-1, and inadequate adiponectin secretion (18,21). These results suggest that ectopic insulin-resistant adipose tissue, particularly in skeletal muscle, could induce insulin resistance in nearby tissues.…”

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confidence: 99%

Insulin Resistance in SHR/NDmc-cp Rats Correlates with Enlarged Perivascular Adipocytes and Endothelial Cell Dysfunction in Skeletal Muscle

Hariya

Mochizuki

Inoue

et al. 2014

J Nutr Sci Vitaminol

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Summary Ectopic adipose tissue in skeletal muscle is implicated in the development of insulin resistance, which is frequently induced by abnormal dietary habits such as excessive eating and a high-fat diet. However, the characteristics of ectopic adipocytes are unknown. In this study, we investigated the characteristics of ectopic adipocytes in the skeletal muscle of spontaneously hypertensive corpulent congenic (SHR/NDmc-cp) rats as a model of insulin resistance from excessive eating. SHR/NDmc-cp rats displayed overt insulin resistance with high plasma glucose, insulin, and triacylglycerol concentrations relative to control Wistar-Kyoto (WKY) rats. In contrast, streptozotocin (STZ)-treated WKY rats had high glucose but low insulin concentrations. Ectopic adipocytes were found around blood vessels in the gastrocnemius in SHR/NDmc-cp rats. Areas of perivascular adipocytes and protein expression of resistin were greater in SHR/NDmc-cp rats than in control and STZ-treated WKY rats. The level of the phosphorylated (active) form of endothelial nitric oxide synthase in the gastrocnemius was lower in SHR/NDmc-cp rats than in the other groups. Insulinresistant SHR/NDmc-cp rats showed enlarged perivascular adipocytes and greater endothelial cell dysfunction in the gastrocnemius.

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Periadventitial Adipose Tissue Plays a Critical Role in Vascular Remodeling

Cited by 184 publications

References 43 publications

A novel lipoprotein (a) lowering drug, D-47, decreases neointima thickening after vascular injury

A novel lipoprotein (a) lowering drug, D-47, decreases neointima thickening after vascular injury

Adipoparacrinology: an Emerging Field in Biomedical Research

Insulin Resistance in SHR/NDmc-cp Rats Correlates with Enlarged Perivascular Adipocytes and Endothelial Cell Dysfunction in Skeletal Muscle

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