Ghrelin Expression in Atherosclerotic Plaques and Perivascular Adipose Tissue: Implications for Vascular Inflammation in Peripheral Artery Disease

Author:

Peiu Sorin Nicolae12,Iosep Diana Gabriela34,Danciu Mihai34ORCID,Scripcaru Veronica4,Ianole Victor4,Mocanu Veronica2ORCID

Affiliation:

1. Vascular Surgery Department, “Grigore T. Popa” University of Medicine and Pharmacy, 700115 Iasi, Romania

2. Morpho-Functional Sciences II (Physiopathology) Department, “Grigore T. Popa” University of Medicine and Pharmacy, 700115 Iasi, Romania

3. Pathology Department, “Sf. Spiridon” Emergency Clinical Hospital, 700111 Iasi, Romania

4. Morpho-Functional Department—Morphopathology, “Grigore T. Popa” University of Medicine and Pharmacy, 700115 Iasi, Romania

Abstract

Atherosclerosis, a leading cause of peripheral artery disease (PAD), is driven by lipid accumulation and chronic inflammation within arterial walls. Objectives: This study investigates the expression of ghrelin, an anti-inflammatory peptide hormone, in plaque morphology and inflammation in patients with PAD, highlighting its potential role in age-related vascular diseases and metabolic syndrome. Methods: The analysis specifically focused on the immunohistochemical expression of ghrelin in atherosclerotic plaques and perivascular adipose tissue (PVAT) from 28 PAD patients. Detailed immunohistochemical staining was performed to identify ghrelin within these tissues, comparing its presence in various plaque types and assessing its association with markers of inflammation and macrophage polarization. Results: Significant results showed a higher prevalence of calcification in fibro-lipid plaques (63.1%) compared to fibrous plaques, with a notable difference in inflammatory infiltration between the two plaque types (p = 0.027). Complicated plaques exhibited increased ghrelin expression, suggesting a modulatory effect on inflammatory processes, although this did not reach statistical significance. The correlation between ghrelin levels and macrophage presence, especially the pro-inflammatory M1 phenotype, indicates ghrelin’s involvement in the inflammatory dynamics of atherosclerosis. Conclusions: The findings propose that ghrelin may influence plaque stability and vascular inflammation, pointing to its therapeutic potential in managing atherosclerosis. The study underlines the necessity for further research to clarify ghrelin’s impact on vascular health, particularly in the context of metabolic syndrome and age-related vascular alterations.

Publisher

MDPI AG

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