Table 3. Experimental evidence relevant to PVAT inflammation in AAA and the models used.
| Conclusions | Models | References |
|
Abbreviations: ANGPTL2, angiopoietin-like protein 2; AT1a, angiotensin Ⅱ type 1a receptor; ATDC, adipose tissue dendritic cell; CCL2, C-C motif chemokine ligand 2; COMP, cartilage oligomeric matrix protein; EGR1, early growth response 1; ET-1, endothelin-1; FABP4, fatty acid-binding protein 4; FSP27, fat-specific protein 27; ICAM-1, intercellular adhesion molecule-1; JNK, c-Jun N-terminal kinase; MC, mast cell; MMP, matrix metalloproteinase; NCC, Na-Cl co-transporter; NE, neutrophil elastase; NF-κB, nuclear factor kappa-B; PDGF-D, platelet-derived growth factor-D; PCNA, proliferating cell nuclear antigen; TGF-β, transforming growth factor-β; Th17, T helper 17; TLR4, Toll-like receptor 4; VSMC, vascular smooth muscle cell. | ||
| Neutrophils are attracted by IL-8 and interact directly with adipocytes through the CD11b-ICAM-1 complex. | Indirect evidence from an obesity model | [38] |
| Neutrophils secrete NE to activate TLR4, thus promoting macrophage recruitment and amplifying inflammation. | Indirect evidence from an obesity model | [39] |
| EGR1 is differentially expressed between AAA and controls and may be associated with MC activation. | Elastase infusion | [41] |
| Obesity promotes the release of CCL2 from PVAT and the accumulation of macrophages. | HFD + Ang Ⅱ | [4] |
| FSP27 facilitates macrophage recruitment via the JNK-CCL2 axis and increases MMP-12. | HFD + Ang Ⅱ | [45] |
| Specific overexpression of SAA in PVAT elevates macrophage infiltration and MMP activity. | HFD + Ang Ⅱ | [48] |
| Leptin and FABP4 upregulate IL-18, the canonical IL-18 receptor (IL-18R), and NCC, an additional IL-18 receptor identified in AAA lesions, thereby promoting IL-18-mediated inflammatory responses. | Ang Ⅱ + Apoe−/− | [50] |
| ATDCs release IL-6, TGF-β, and IL-23, promoting the differentiation of Th17 cells. | Indirect evidence from an obesity model | [51] |
| Ceramides recruit T cells, and leukocytes likely migrate to aneurysms from the post-capillary venules in PVAT. | Ang Ⅱ + Apoe−/− | [33] |
| Overexpression of ET-1 promotes the infiltration of macrophages and secretion of MMP-2. | HFD + Apoe−/− | [61] |
| AT1a receptor activation promotes M1 polarization and enhances MMP-2 and MMP-9 through OPN. | Ang Ⅱ + Apoe−/− | [62] |
| ANGPTL2 from macrophages could activate the NF-κB cascade and upregulate MMP-9 expression. | CaCl2 | [63] |
| Adventitial mast cells can enhance macrophage-derived MMP-9 production through direct contact or IFN-γ signaling. | CaCl2 | [64] |
| PDGF-D spurs adventitial fibroblast activation via the TGF-β/Smad pathway and exacerbates CD68+ macrophage infiltration. | HFD + Ang Ⅱ | [65] |
| Leptin activates p38 MAPK signaling, downregulating the differentiation markers and upregulating the PCNA in VSMCs. | Indirect evidence from an obesity model | [68] |
| COMP could significantly increase survivin protein in VSMCs and reduce VSMC apoptosis. | CaCl2 | [74] |
| CCL2 mediated the chemoattractant effect of apoptotic VSMCs and triggered macrophage infiltration during SMC death. | Ang Ⅱ + Apoe−/− | [75] |