Perivascular adipose tissue: Fine-tuner of vascular redox status and inflammation

Cheng, Chak Kwong; Ding, Huanyu; Jiang, Minchun; Yin, Huiyong; Gollasch, Maik; Huang, Yü

doi:10.1016/j.redox.2023.102683

Cited by 20 publications

(12 citation statements)

References 113 publications

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“…Excessive accumulation of triglycerides in PVAT leads to enlarge adipocytes due to excess lipid droplets. WAT is responsible for the storage of excessive energy in the form of lipids (large single droplets), while BAT stores large amounts of lipids due to its thermogenic property (contains multiple smaller lipid droplets) ( 10 , 21 ). In our study, HFD not only elevated the circulating lipid concentrations but also increased the average size of lipid droplets in PVAT.…”

Section: Discussionmentioning

confidence: 99%

“…Whitening of PVAT during obesity represents excessive production of free radicals and subsequent occurrence of oxidative stress. In contrast to BAT-like characteristics, whitening of PVAT shows larger lipid droplets, lower expression of uncoupling protein-1 (UCP-1), and low mitochondrial number ( 10 ). This phenomenon is accompanied by an increased inflammatory response, which decreases the vascular relaxation response, regulated by PVAT ( 11 ).…”

Section: Introductionmentioning

confidence: 93%

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Exercise attenuates high-fat diet-induced PVAT dysfunction through improved inflammatory response and BMP4-regulated adipose tissue browning

Liu,

Jiang,

et al. 2024

Front. Nutr.

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BackgroundPerivascular adipose tissue (PVAT) dysfunction impairs vascular homeostasis. Impaired inflammation and bone morphogenetic protein-4 (BMP4) signaling are involved in thoracic PVAT dysfunction by regulating adipokine secretion and adipocyte phenotype transformation. We investigated whether aerobic exercise training could ameliorate high-fat diet (HFD)-induced PVAT dysfunction via improved inflammatory response and BMP4-mediated signaling pathways.MethodsSprague-Dawley rats (n = 24) were divided into three groups, namely control, high-fat diet (HFD), and HFD plus exercise (HEx). After a 6-week intervention, PVAT functional efficiency and changes in inflammatory biomarkers (circulating concentrations in blood and mRNA expressions in thoracic PVAT) were assessed.ResultsChronic HFD feeding caused obesity and dyslipidemia in rats. HFD decreased the relaxation response of PVAT-containing vascular rings and impaired PVAT-regulated vasodilatation. However, exercise training effectively reversed these diet-induced pathological changes to PVAT. This was accompanied by significantly (p < 0.05) restoring the morphological structure and the decreased lipid droplet size in PVAT. Furthermore, HFD-induced impaired inflammatory response (both in circulation and PVAT) was notably ameliorated by exercise training (p < 0.05). Specifically, exercise training substantially reversed HFD-induced WAT-like characteristics to BAT-like characteristics as evidenced by increased UCP1 and decreased FABP4 protein levels in PVAT against HFD. Exercise training promoted transcriptional activation of BMP4 and associated signaling molecules (p38/MAPK, ATF2, PGC1α, and Smad5) that are involved in browning of adipose tissue. In conjunction with gene expressions, exercise training increased BMP4 protein content and activated downstream cascades, represented by upregulated p38/MAPK and PGC1α proteins in PVAT.ConclusionRegular exercise training can reverse HFD-induced obesity, dyslipidemia, and thoracic PVAT dysfunction in rats. The browning of adipose tissue through exercise appears to be modulated through improved inflammatory response and/or BMP4-mediated signaling cascades in obese rats.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 93%

Exercise attenuates high-fat diet-induced PVAT dysfunction through improved inflammatory response and BMP4-regulated adipose tissue browning

Liu,

Jiang,

et al. 2024

Front. Nutr.

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“…Its primary role involves creating a localized inflammatory microenvironment by facilitating the infiltration of inflammatory cells into the vessel wall and inducing vascular remodeling. Consequently, this process contributes to or exacerbates local pathological changes in the vasculature 13 – 15 . Nonetheless, the precise underlying mechanism through which inflammatory PVAT contributes to the pathogenesis of AD remains elusive.…”

Section: Introductionmentioning

confidence: 99%

The role of RUNX1/NF-κB in regulating PVAT inflammation in aortic dissection

Wang,

Dong,

Liu

et al. 2024

Sci Rep

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The pathogenesis of aortic dissection (AD), an aortic disease associated with high mortality, involves significant vascular inflammatory infiltration. However, the precise relationship between perivascular adipose tissue (PVAT) and aortic dissection remains incompletely understood. The objective of this study is to investigate the role of PVAT inflammation in the pathogenesis of aortic dissection and identify novel therapeutic targets for this disease. The mouse model of aortic dissection was established in this study through intraperitoneal injection of Ang II and administration of BAPN in drinking water. Additionally, control groups were established at different time points including the 2-week group, 3-week group, and 4-week group. qPCR and immunohistochemistry techniques were employed to detect the expression of inflammatory markers and RUNX1 in PVAT surrounding the thoracic aorta in mice. Additionally, an aortic dissection model was established using RUNX1 knockout mice, and the aforementioned indicators were assessed. The 3T3-L1 cells were induced to differentiate into mature adipocytes in vitro, followed by lentivirus transfection for the knockdown or overexpression of RUNX1. The study aimed to investigate the potential cell-to-cell interactions by co-culturing 3T3-L1 cells with A7r5 or RAW264.7 cells. Subsequently, human aortic PVAT samples were obtained through clinical surgery and the aforementioned indicators were detected. In comparison to the control group, the aortic dissection model group exhibited decreased expression of MMP-2 and NF-κB in PVAT, while TNF-α and RUNX1 expression increased. Suppression of RUNX1 expression resulted in increased MMP-2 and NF-κB expression in PVAT, along with decreased TNF-α expression. Overexpression of RUNX1 upregulated the expression levels of NF-Κb, MMP-2, and TNF-α in adipocytes, whereas knockdown of RUNX1 exerted an opposite effect. Macrophages co-cultured with adipocytes overexpressing RUNX1 exhibited enhanced CD86 expression, while vascular smooth muscle cells co-cultured with these adipocytes showed reduced α-SMA expression. In human samples, there was an increase in both RUNX1 and MMP-2 expression levels, accompanied by a decrease in TNF-α and NF-Κb expression. The presence of aortic dissection is accompanied by evident inflammatory alterations in the PVAT, and this phenomenon appears to be associated with the involvement of RUNX1. It is plausible that the regulation of PVAT's inflammatory changes by RUNX1/NF-κB signaling pathway plays a role in the pathogenesis of aortic dissection.

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“…Their precise regulation of production in the endothelium is crucial for controlling various cell functions in the vascular system [2][3][4]. Otherwise, excessive production of ROS (including superoxide O 2 _ , hydroxyl radical _ OH, and peroxynitrite anion ONOO _ ) can cause the disruption of redox homeostasis, damage the immune system response, and favour the manifestation of vascular diseases [5,6]. This situation can occur in various circumstances where there is an imbalance between ROS generation and antioxidant defence mechanisms, such as chronic inflammation, ischemia-reperfusion injury, aging, and metabolic disorders.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin Regulation of Vascular Homeostasis: Exploring the Role of ROS and RAS Blockers

Koumallos

Sigala

Milas

et al. 2023

IJMS

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Extensive research has been conducted to elucidate and substantiate the crucial role of the Renin-Angiotensin System (RAS) in the pathogenesis of hypertension, cardiovascular disorders, and renal diseases. Furthermore, the role of oxidative stress in maintaining vascular balance has been well established. It has been observed that many of the cellular effects induced by Angiotensin II (Ang II) are facilitated by reactive oxygen species (ROS) produced by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. In this paper, we present a comprehensive overview of the role of ROS in the physiology of human blood vessels, specifically focusing on its interaction with RAS. Moreover, we delve into the mechanisms by which clinical interventions targeting RAS influence redox signaling in the vascular wall.

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Perivascular adipose tissue: Fine-tuner of vascular redox status and inflammation

Cited by 20 publications

References 113 publications

Exercise attenuates high-fat diet-induced PVAT dysfunction through improved inflammatory response and BMP4-regulated adipose tissue browning

Exercise attenuates high-fat diet-induced PVAT dysfunction through improved inflammatory response and BMP4-regulated adipose tissue browning

The role of RUNX1/NF-κB in regulating PVAT inflammation in aortic dissection

Angiotensin Regulation of Vascular Homeostasis: Exploring the Role of ROS and RAS Blockers

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