Literature DB >> 25770816

Collaterals: Implications in cerebral ischemic diseases and therapeutic interventions.

Yasuo Nishijima1, Yosuke Akamatsu1, Phillip R Weinstein2, Jialing Liu3.   

Abstract

Despite the tremendous progress made in the treatment of cerebrovascular occlusive diseases, many patients suffering from ischemic brain injury still experience dismal outcomes. Although rehabilitation contributes to post-stroke functional recovery, there is no doubt that interventions that promote the restoration of blood supply are proven to minimize ischemic injury and improve recovery. In response to the acutely decreased blood perfusion during arterial occlusion, arteriogenesis, the compensation of blood flow through the collateral circulation during arterial obstructive diseases can act not only in a timely fashion but also much more efficiently compared to angiogenesis, the sprouting of new capillaries, and a mechanism occurring in a delayed fashion while increases the total resistance of the vascular bed of the affected territory. Interestingly, despite the vast differences between the two vascular remodeling mechanisms, some crucial growth factors and cytokines involved in angiogenesis are also required for arteriogenesis. Understanding the mechanisms underlying vascular remodeling after ischemic brain injury is a critical step towards the development of effective therapies for ischemic stroke. The present article will discuss our current views in vascular remodeling acutely after brain ischemia, namely arteriogenesis, and some relevant clinical therapies available on the horizon in augmenting collateral flow that hold promise in treating ischemic brain injury. This article is part of a Special Issue entitled SI: Cell Interactions In Stroke. Published by Elsevier B.V.

Entities:  

Keywords:  Anastomosis; Angiogenesis; Arteriogenesis; Carotid disease; Stroke; Vascular remodeling

Mesh:

Year:  2015        PMID: 25770816      PMCID: PMC4567541          DOI: 10.1016/j.brainres.2015.03.006

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


  136 in total

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5.  Impaired Collateral Flow Compensation During Chronic Cerebral Hypoperfusion in the Type 2 Diabetic Mice.

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10.  TIMP3 attenuates cerebral ischemia/reperfusion-induced apoptosis and oxidative stress in neurocytes by regulating the AKT pathway.

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