PMID- 32798552
OWN - NLM
STAT- MEDLINE
DCOM- 20201215
LR  - 20201215
IS  - 1095-9319 (Electronic)
IS  - 0026-2862 (Linking)
VI  - 132
DP  - 2020 Nov
TI  - Recruitment and maturation of the coronary collateral circulation: Current 
      understanding and perspectives in arteriogenesis.
PG  - 104058
LID - S0026-2862(20)30118-7 [pii]
LID - 10.1016/j.mvr.2020.104058 [doi]
AB  - The coronary collateral circulation is a rich anastomotic network of primitive 
      vessels which have the ability to augment in size and function through the 
      process of arteriogenesis. In this review, we evaluate the current understandings 
      of the molecular and cellular mechanisms by which this process occurs, 
      specifically focussing on elevated fluid shear stress (FSS), inflammation, the 
      redox state and gene expression along with the integrative, parallel and 
      simultaneous process by which this occurs. The initiating step of arteriogenesis 
      occurs following occlusion of an epicardial coronary artery, with an increase in 
      FSS detected by mechanoreceptors within the endothelium. This must occur within a 
      'redox window' where an equilibrium of oxidative and reductive factors are 
      present. These factors initially result in an inflammatory milieu, mediated by 
      neutrophils as well as lymphocytes, with resultant activation of a number of 
      downstream molecular pathways resulting in increased expression of proteins 
      involved in monocyte attraction and adherence; namely vascular cell adhesion 
      molecule 1 (VCAM-1), monocyte chemoattractant protein 1 (MCP-1) and transforming 
      growth factor beta (TGF-beta). Once monocytes and other inflammatory cells adhere to 
      the endothelium they enter the extracellular matrix and differentiate into 
      macrophages in an effort to create a favourable environment for vessel growth and 
      development. Activated macrophages secrete inflammatory cytokines such as tumour 
      necrosis factor-alpha (TNF-alpha), growth factors such as fibroblast growth factor-2 
      (FGF-2) and matrix metalloproteinases. Finally, vascular smooth muscle cells 
      proliferate and switch to a contractile phenotype, resulting in an increased 
      diameter and functionality of the collateral vessel, thereby allowing improved 
      perfusion of the distal myocardium subtended by the occluded vessel. This 
      simultaneously reduces FSS within the collateral vessel, inhibiting further 
      vessel growth.
CI  - Copyright (c) 2020 Elsevier Inc. All rights reserved.
FAU - Allahwala, Usaid K
AU  - Allahwala UK
AD  - Department of Cardiology, Royal North Shore Hospital, Sydney, Australia; The 
      University of Sydney, Sydney, Australia. Electronic address: 
      usaid.allahwala@sydney.edu.au.
FAU - Khachigian, Levon M
AU  - Khachigian LM
AD  - Vascular Biology and Translational Research, School of Medical Sciences, 
      University of New South Wales, Sydney, Australia.
FAU - Nour, Daniel
AU  - Nour D
AD  - Department of Cardiology, Royal North Shore Hospital, Sydney, Australia.
FAU - Ridiandres, Anisyah
AU  - Ridiandres A
AD  - The University of Sydney, Sydney, Australia.
FAU - Billah, Muntasir
AU  - Billah M
AD  - The University of Sydney, Sydney, Australia.
FAU - Ward, Michael
AU  - Ward M
AD  - Department of Cardiology, Royal North Shore Hospital, Sydney, Australia.
FAU - Weaver, James
AU  - Weaver J
AD  - Cardiology Department, Royal Prince Alfred Hospital, Sydney, Australia; The 
      University of New South Wales, Australia.
FAU - Bhindi, Ravinay
AU  - Bhindi R
AD  - Department of Cardiology, Royal North Shore Hospital, Sydney, Australia; The 
      University of Sydney, Sydney, Australia.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20200813
PL  - United States
TA  - Microvasc Res
JT  - Microvascular research
JID - 0165035
RN  - 0 (Angiogenic Proteins)
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
SB  - IM
MH  - Angiogenic Proteins/metabolism
MH  - Animals
MH  - Chronic Disease
MH  - *Collateral Circulation
MH  - *Coronary Circulation
MH  - Coronary Occlusion/metabolism/*physiopathology
MH  - Coronary Vessels/metabolism/*physiopathology
MH  - Cytokines
MH  - Humans
MH  - Inflammation Mediators/metabolism
MH  - Mechanoreceptors/metabolism
MH  - Mechanotransduction, Cellular
MH  - *Neovascularization, Physiologic
MH  - Oxidative Stress
MH  - *Vascular Remodeling
OTO - NOTNLM
OT  - Arteriogenesis
OT  - Chronic total occlusion
OT  - Collateral circulation
OT  - Collaterals
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2020/08/18 06:00
MHDA- 2020/12/16 06:00
CRDT- 2020/08/18 06:00
PHST- 2020/01/09 00:00 [received]
PHST- 2020/06/09 00:00 [revised]
PHST- 2020/08/11 00:00 [accepted]
PHST- 2020/08/18 06:00 [pubmed]
PHST- 2020/12/16 06:00 [medline]
PHST- 2020/08/18 06:00 [entrez]
AID - S0026-2862(20)30118-7 [pii]
AID - 10.1016/j.mvr.2020.104058 [doi]
PST - ppublish
SO  - Microvasc Res. 2020 Nov;132:104058. doi: 10.1016/j.mvr.2020.104058. Epub 2020 Aug 
      13.