Vascular Macrophages as Therapeutic Targets to Treat Intracranial Aneurysms

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Muhammad , S , Chaudhry , S R , Dobreva , G , Lawton , M T , Niemelä , M & Hänggi , D 2021 , ' Vascular Macrophages as Therapeutic Targets to Treat Intracranial Aneurysms ' , Frontiers in Immunology , vol. 12 , 630381 . https://doi.org/10.3389/fimmu.2021.630381

Title: Vascular Macrophages as Therapeutic Targets to Treat Intracranial Aneurysms
Author: Muhammad, Sajjad; Chaudhry, Shafqat Rasul; Dobreva, Gergana; Lawton, Michael T.; Niemelä, Mika; Hänggi, Daniel
Contributor organization: HUS Neurocenter
Clinicum
Neurokirurgian yksikkö
University of Helsinki
Department of Neurosciences
Date: 2021-03-08
Language: eng
Number of pages: 9
Belongs to series: Frontiers in Immunology
ISSN: 1664-3224
DOI: https://doi.org/10.3389/fimmu.2021.630381
URI: http://hdl.handle.net/10138/329401
Abstract: Aneurysmal subarachnoid hemorrhage (aSAH) is a highly fatal and morbid type of hemorrhagic strokes. Intracranial aneurysms (ICAs) rupture cause subarachnoid hemorrhage. ICAs formation, growth and rupture involves cellular and molecular inflammation. Macrophages orchestrate inflammation in the wall of ICAs. Macrophages generally polarize either into classical inflammatory (M1) or alternatively-activated anti-inflammatory (M2)-phenotype. Macrophage infiltration and polarization toward M1-phenotype increases the risk of aneurysm rupture. Strategies that deplete, inhibit infiltration, ameliorate macrophage inflammation or polarize to M2-type protect against ICAs rupture. However, clinical translational data is still lacking. This review summarizes the contribution of macrophage led inflammation in the aneurysm wall and discuss pharmacological strategies to modulate the macrophageal response during ICAs formation and rupture.
Subject: intracranial aneurysms
monocytes
macrophages
inflammation
subarachnoid hemorrhage
stroke
macrophage polarization
3121 General medicine, internal medicine and other clinical medicine
3112 Neurosciences
Peer reviewed: Yes
Rights: cc_by
Usage restriction: openAccess
Self-archived version: publishedVersion


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