Education, Science, Technology, Innovation and Life
Open Access
Sign In

Progress of macrophage polarization in the treatment of aortic dissection

Download as PDF

DOI: 10.23977/medbm.2024.020114 | Downloads: 8 | Views: 125


Zilin Lu 1, Yubing He 2, Ning Wang 2, Jian Dong 2, Zheng Shu 2


1 School of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai, 200093, China
2 Department of Vascular Surgery, Shanghai TCM-Integrated Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200082, China

Corresponding Author

Jian Dong


Aortic dissection is one of the most devastating cardiovascular diseases. One of the most important pathological features of aortic dissection is local inflammatory response, including the infiltration of inflammatory cells, extracellular matrix degradation, and smooth muscle cell phenotype switch. Macrophages which are the core of the inflammatory response play an extremely pivotal role in the progression of inflammation and tissue remodeling. Macrophages can be artificially divided into M1 and M2 types, of which the M1-type promotes inflammation while the M2-type is associated with the regression of inflammation and tissue healing. Mastering the switch of phenotypic transformation of macrophages may be of great help in inhibiting the inflammation of aortic tissue and facilitating tissue healing, as well as the treatment of aortic dissection. In this paper, we focus on the polarization of macrophages and discuss the role of macrophages in aortic dissection, the polarization pathway and the effect of related polarizing agents on the treatment of aortic dissection.


Macrophage polarization, Aortic dissection, Inflammation, review


Zilin Lu, Yubing He, Ning Wang, Jian Dong, Zheng Shu, Progress of macrophage polarization in the treatment of aortic dissection. MEDS Basic Medicine (2024) Vol. 2: 109-113. DOI:


[1] Evangelista A, Isselbacher EM, Bossone E, et al. Insights From the International Registry of Acute Aortic Dissection: A 20-Year Experience of Collaborative Clinical Research.[J]. Circulation. 2018; 137(17):1846-1860. 
[2] Li X, Liu D, Zhao L, et al. Targeted depletion of monocyte/ macrophage suppresses aortic dissection with the spatial regulation of MMP-9 in the aorta. [J]. Life Sci, 2020, 254: 116927.
[3] Peterson KR, Cottam MA, Kennedy AJ, et al. Macrophage-targeted therapeutics for metabolic disease[J].Trends Pharmacol Sci, 2018, 39(6): 536-546.
[4] Sica A, Mantovani A. Macrophage plasticity and polarization: In vivo veritas [J]. J Clin Invest, 2012, 122(3): 787-795. 
[5] Rahman K, Fisher EA. Insights from pre-clinical and clinical studies on the role of innate inflammation in atherosclerosis regression. Front Cardiovasc Med, 2018, 5: 32.
[6] Wang X, Zhang H, Cao L, et al. The role of macrophages in aortic dissection. [J]. Front Physiol, 2020, 11: 54.
[7] Cameron, Amy R et al. "Anti-Inflammatory Effects of Metformin Irrespective of Diabetes Status."[J]. Circulation research vol. 119, 5 (2016): 652-665.
[8] Hu G, Guo M, Xu J, et al. Nanoparticles targeting macrophages as potential clinical therapeutic agents against cancer and inflammation. [J]. Front Immunol, 2019, 10: 1998.
[9] Adam M, Kooreman NG, Jagger A, et al. Systemic upregulation of IL-10 (interleukin-10) using a nonimmunogenic vector reduces growth and rate of dissecting abdominal aortic aneurysm.[J]. Arterioscler Thromb Vasc Biol, 2018, 38(8): 1796-1805.
[10] Scola L, Di Maggio FM, Vaccarino L, et al. Role of TGF-β pathway polymorphisms in sporadic thoracic aortic aneurysm: Rs900 TGF- β2 is a marker of differential gender susceptibility. [J]. Mediators Inflamm, 2014, 2014: 165758.
[11] Bi C, Fu Y, Li B. Brain-derived neurotrophic factor alleviates diabetes mellitus-accelerated atherosclerosis by promoting M2 polarization of macrophages through repressing the STAT3 pathway.[J]. Cell Signal, 2020, 70: 109569.
[12] Svendsen P, Graversen JH, Etzerodt A, et al. Antibody-directed glucocorticoid targeting to CD163 in M2-type macrophages attenuates fructose-induced liver inflammatory changes. [J]. Mol Ther Methods Clin Dev, 2016, 4: 50-61.
[13] Razavi MK, Donohoe D, D'Agostino RB, et al. Adventitial drug delivery of dexamethasone to improve primary patency in the treatment of superficial femoral and popliteal artery disease: 12- month results from the DANCE clinical trial. [J]. JACC Cardiovasc Interv, 2018, 11(10): 921-931.
[14] Zhang L, Zhou J, Jing Z, et al. Glucocorticoids regulate the vascular remodeling of aortic dissection via the p38 MAPK-HSP27 pathway mediated by soluble TNF-RII.[J]. EBioMedicine, 2018, 27: 247-257.
[15] Zhang G, Xue H, Sun D, et al. Soft apoptotic-cell-inspired nanoparticles persistently bind to macrophage membranes and promote anti-inflammatory and pro-healing effects. [J]. Acta Biomater, 2021, 131: 452-463.
[16] Andreata F, Syvannarath V, Clement M, et al. Macrophage CD31 signaling in dissecting aortic aneurysm. [J]. J Am Coll Cardiol, 2018, 72(1): 45-57.
[17] Wang Z, Brandt S, Medeiros A, et al. MicroRNA 21 is a homeostatic regulator of macrophage polarization and prevents prostaglandin E2-mediated M2 generation.[J]. PLoS One, 2015, 10(2): e0115855.
[18] Xue YL, Zhang SX, Zheng CF, et al. Long non-coding RNA MEG3 inhibits M2 macrophage polarization by activating TRAF6 via microRNA-223 down-regulation in viral myocarditis.[J]. J Cell Mol Med, 2020, 24(21): 12341-12354.
[19] Martinez B, Peplow PV. Immunomodulators and microRNAs as neurorestorative therapy for ischemic stroke.[J]. Neural Regen Res, 2017, 12(6): 865-874
[20] Di Gregoli K, Mohamad Anuar NN, Bianco R, et al. MicroRNA- 181b controls atherosclerosis and aneurysms through regulation of TIMP-3 and elastin. [J]. Circ Res, 2017, 120(1): 49-65.
[21] Essandoh K, Li Y, Huo J, et al. MiRNA-mediated macrophage polarization and its potential role in the regulation of inflammatory response. [J]. Shock, 2016, 46(2): 122-131.
[22] Ota K, Dambaeva S, Kim MW, et al. 1, 25-dihydroxy-vitamin D3 regulates NK-cell cytotoxicity, cytokine secretion, and degranulation in women with recurrent pregnancy losses. [J]. Eur J Immunol, 2015, 45(11): 3188-3199.
[23] Shojadoost B, Behboudi S, Villanueva AI, et al. Vitamin D3 modulates the function of chicken macrophages. [J]. Res Vet Sci, 2015, 100: 45-51.
[24] Manson JE, Bassuk SS, Cook NR, et al. Vitamin D, marine n-3 fatty acids, and primary prevention of cardiovascular disease current evidence. [J]. Circ Res, 2020, 126(1): 112-128.
[25] Legarth C, Grimm D, Krüger M, et al. Potential beneficial effects of vitamin d in coronary artery disease. [J]. Nutrients, 2019, 12(1): 99.

Downloads: 456
Visits: 14649

Sponsors, Associates, and Links

All published work is licensed under a Creative Commons Attribution 4.0 International License.

Copyright © 2016 - 2031 Clausius Scientific Press Inc. All Rights Reserved.