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Review
. 2021 Mar 21;10(6):1291.
doi: 10.3390/jcm10061291.

Perirenal Adipose Tissue-Current Knowledge and Future Opportunities

Affiliations
Review

Perirenal Adipose Tissue-Current Knowledge and Future Opportunities

Adriana Grigoraș et al. J Clin Med. .

Abstract

The perirenal adipose tissue (PRAT), a component of visceral adipose tissue, has been recently recognized as an important factor that contributes to the maintenance of the cardiovascular system and kidney homeostasis. PRAT is a complex microenvironment consisting of a mixture of white adipocytes and dormant and active brown adipocytes, associated with predipocytes, sympathetic nerve endings, vascular structures, and different types of inflammatory cells. In this review, we summarize the current knowledge about PRAT and discuss its role as a major contributing factor in the pathogenesis of hypertension, obesity, chronic renal diseases, and involvement in tumor progression. The new perspectives of PRAT as an endocrine organ and recent knowledge regarding the possible activation of dormant brown adipocytes are nowadays considered as new areas of research in obesity, in close correlation with renal and cardiovascular pathology. Supplementary PRAT complex intervention in tumor progression may reveal new pathways involved in carcinogenesis and, implicitly, may identify additional targets for tailored cancer therapy.

Keywords: cardiovascular diseases; chronic kidney disease; obesity; perirenal adipose tissue.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic diagram of perirenal adipose tissue involvement in pathology. FFAs—free fatty acids; MCP-1—monocyte chemoattractant protein-1; SRAA—renin-angiotensin-aldosterone system; TGs—triglycerides; TNF-α—tumor necrosis factor-α; ↑—increased level.
Figure 2
Figure 2
Hypothetical pathways of perirenal adipose tissue (PRAT) induced tumor progression. HOXC8—homeobox protein 8; HOXC9—homeobox protein 9; IL-6—interleukin 6; PRAT—perirenal adipose tissue; TNF-α—tumor necrosis factor-α; UCP-1—uncoupling protein 1; ↑—increased level; ↓—decreased level; ?—unknown.

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