Cardiovascular Disease and Adiposity / Eicosanoids and Hypertension Pharmacology · Journal article
Biomedicines · August 11, 2026
Raises a question worth testing. It does not answer one.
This is a narrative review that identifies perirenal adipose tissue (PRAT) as a clinically relevant endocrine organ linking obesity to cardiovascular disease through RAAS activation, adipokine dysregulation, and microRNA-mediated inflammation. The review proposes multiple therapeutic strategies—ranging from established interventions (lifestyle, RAAS inhibitors) to exploratory approaches (senotherapy, ADMSC bioengineering, microbiota modulation)—but presents no original clinical data, effect sizes, or comparative efficacy evidence.
Narrative review.
PRAT expansion is associated with activation of the renin–angiotensin–aldosterone system (RAAS), increasing blood pressure Adipokine dysregulation and overexpression of miR-24-3p, miR-155, miR-146a, and miR-21 in PRAT modulate inflammation and oxidative stress PRAT thickness assessment via computed tomography, magnetic resonance, or ultrasound has emerged as a complementary measure for CVD risk evaluation
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This review identifies PRAT as a therapeutic target and suggests imaging assessment may complement existing cardiovascular risk stratification in patients with obesity. However, the absence of clinical trial data or outcome evidence means clinicians cannot yet adopt these insights as practice changes; the review identifies research directions rather than established clinical recommendations.
A narrative review synthesizing mechanistic insights and potential therapeutic targets for perirenal adipose tissue in cardiovascular disease, without original data or clinical trial evidence.
As stated by the source record.
This review identifies PRAT as a therapeutic target and suggests imaging assessment may complement existing cardiovascular risk stratification in patients with obesity. However, the absence of clinical trial data or outcome evidence means clinicians cannot yet adopt these insights as practice changes; the review identifies research directions rather than established clinical recommendations.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Perirenal adipose tissue (PRAT) has emerged as a clinically relevant endocrine organ connecting obesity to cardiovascular disease (CVD), chronic kidney disease, and certain malignancies. Its unique anatomical location, surrounding the kidneys, accounts for PRAT’s role in altering intrarenal haemodynamics and hydrostatic pressure. Accordingly, PRAT’s expansion is associated with the activation of the renin–angiotensin–aldosterone system (RAAS), further increasing blood pressure. Adipokine dysregulation, together with overexpression of miR-24-3p, miR-155, miR-146a, and miR-21 in PRAT, modulates inflammation and oxidative stress, leading to endothelial dysfunction and increased risk of atherosclerosis and hypertension in obesity. Imaging assessment of PRAT thickness through computed tomography, magnetic resonance, or ultrasound has also emerged as a complementary measure for the evaluation of CVD risk. Potential therapeutic strategies targeting PRAT include lifestyle interventions, antidiabetic agents, RAAS inhibitors, adipose tissue browning agents, NOD-like receptor protein 3 (NLRP3) inflammasome inhibitors, peroxisome proliferator-activated receptor gamma (PPARγ) agonists, and surgery. Currently, novel therapeutic interventions targeting PRAT activity in CVD, such as senotherapeutic strategies, bioengineering approaches aimed at enhancing adipose-derived mesenchymal stem cell (ADMSC) function, gut microbiota modulation, and colchicine and bone morphogenetic protein 4 (BMP4) administration, are also being explored. In light of these findings, PRAT’s clinical relevance extends beyond its energy storage role, highlighting it as a metabolically active fat depot. Its assessment and therapeutic modulation may complement existing cardiovascular prevention strategies, particularly in patients with obesity.
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