LEADER 01525nam0 22003371i 450 001 UON00154224 005 20231205102935.68 100 $a20020124d1956 |0itac50 ba 101 $aper 102 $aIR 105 $a|||| 1|||| 200 1 $aAgaz va anjam-e "Tazkere"$fXaje Nasir ad-Din Tusi$g[a cura di] Iraj Afsar 210 $aTehran$cEntesarat-e Danesgah-e Tehran$d1335h [1956] 215 $a50 p.$d24 cm 410 1$1001UON00149887$12001 $aEntesharat-e daneshgah-e Tehran$dPublications de l'Université de Tehran$v301 606 $aFILOSOFIA ISLAMICA$xIran$3UONC001439$2FI 620 $aIR$dTihra?n$3UONL005570 686 $aIRA VII A$cIRAN - FILOSOFIA E RELIGIONE - SCIENZE FILOSOFICHE$2A 700 1$aTUSI$bNasiroddin Mohammad ebn Mohammad$3UONV012041$0639685 702 1$aAFSAR$bIraj$3UONV001543 712 $aEntesharat-e daneshgah-e Tehran$3UONV262120$4650 790 0$aNASIRODDIN TUSI$zTUSI, Nasiroddin Mohammad ebn Mohammad$3UONV038445 790 1$aAFSHAR, Iraj$zAFSAR, Iraj$3UONV007474 801 $aIT$bSOL$c20240220$gRICA 899 $aSIBA - SISTEMA BIBLIOTECARIO DI ATENEO$2UONSI 912 $aUON00154224 950 $aSIBA - SISTEMA BIBLIOTECARIO DI ATENEO$dSI IRA VII A 033 $eSI MR 59009 7 033 966 $aFILOSOFIA - IRAN$zFILOSOFIA ISLAMICA - Iran$3UONC016728 966 $aFILOSOFIA PERSIANA$zFILOSOFIA ISLAMICA - Iran$3UONC006139 996 $aAgaz va anjam-e "Tazkere"$91273772 997 $aUNIOR LEADER 04801nam 2200457z- 450 001 9910557600203321 005 20211118 035 $a(CKB)5400000000043675 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/73741 035 $a(oapen)doab73741 035 $a(EXLCZ)995400000000043675 100 $a20202111d2020 |y 0 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 00$aTargeting Monocytes/Macrophages to Treat Atherosclerotic Inflammation 210 $cFrontiers Media SA$d2020 215 $a1 online resource (127 p.) 311 08$a2-88963-599-6 330 $aIt is by now widely recognized that atherosclerosis - with its burden of consequences in cerebro- and cardiovascular diseases - is just a chronic inflammatory process of the arterial wall. A very peculiar, complex and as yet still poorly understood process, upon which hundreds of scientists from several different fields are continuously concentrating their investigative efforts in search of possible leads to therapeutic approaches. Initiation of the disease is given by deposition of lipid in the intimal layers, resulting in endothelial activation and infiltration of blood-derived mononuclear cells. These mature into macrophages, become activated, express scavenger receptors such as SR-A and CD36 and ingest the oxidized lipoprotein accumulating in the lesion. Macrophages thus represent an obvious target for intervention, as they play a crucial role in the progression of the atherosclerotic inflammation. Studies have shown that hypercholesterolaemia can increase monocyte mobilisation from bone marrow into the circulation, and several chemokines and their receptors are involved in the recruitment of blood borne monocytes into the arterial wall. Monocyte-derived macrophages are capable of sustaining their local proliferation, but resident macrophages possibly also participate in progression of the disease. Remarkably, smooth muscle cells can acquire macrophage-like features during atherogenesis, including the ability to uptake lipid, thus becoming a significant proportion of the CD68+ so called 'foam cells'. Lipid-laden macrophages induce extracellular matrix degradation, while lipid uptake eventually causes their death with formation of a necrotic core. The efficiency in clearance of dead cells by phagocytes (efferocytosis), can also be considered as a determinant of plaque vulnerability. An important feature of macrophages is their great plasticity and functional diversity in response to signals from the plaque microenvironment. Several such 'signals' (cholesterol, oxidative stress, hypoxia, cytokines...) can in fact modulate cell differentiation at transcriptional and epigenetic levels, thus altering the balance between the effector vs. reparative functions of macrophages. A whole gamut of specific subsets are thus originated, which appear to be simultaneously present in lesions with proportions that vary according to their location, the disease stage, and the presence of additional cell types such as e.g. dendritic cells. The result is a multiplicity of potential pharmacological targets, representing a major obstacle for the devisement of therapeutic strategies. Experimental approaches have been attempted in diverse directions: e.g. modulating the macrophage phenotype to an anti-inflammatory and resolving state, or blocking pro-inflammatory cytokines that macrophages produce, or alternatively enhancing efferocytosis in order to favour the resolution of inflammation and stabilization of plaques. Blocking monocyte recruitment was proposed in order to hinder the initial steps of atherogenesis. Other treatments were aimed to inhibiting local proliferation of pro-inflammatory macrophages. Specific targeting of macrophages has however to date not yet provided significant, translational results. The present Research Topic collects articles to help unravel the complexity of macrophage behaviour in atherosclerosis and identify innovative pharmacological approaches. 606 $aPharmacology$2bicssc 606 $aScience: general issues$2bicssc 610 $aatherosclerosis progression 610 $afoam cell formation 610 $ainflammation 610 $amonocytes/macrophages 610 $asmooth muscle cells 615 7$aPharmacology 615 7$aScience: general issues 700 $aCorti$b Alessandro$4edt$01302161 702 $aGaucher$b Caroline$4edt 702 $aPompella$b Alfonso$4edt 702 $aCorti$b Alessandro$4oth 702 $aGaucher$b Caroline$4oth 702 $aPompella$b Alfonso$4oth 906 $aBOOK 912 $a9910557600203321 996 $aTargeting Monocytes$93026183 997 $aUNINA