Preprint Review Version 1 This version is not peer-reviewed

Why Should Growth Hormone (GH) Be Considered a Promising Therapeutic Agent for Arteriogenesis? Insights from the GHAS Trial

Version 1 : Received: 29 November 2019 / Approved: 30 November 2019 / Online: 30 November 2019 (10:14:06 CET)

How to cite: Caicedo, D.; Devesa, P.; Alvarez, C.; Devesa, J. Why Should Growth Hormone (GH) Be Considered a Promising Therapeutic Agent for Arteriogenesis? Insights from the GHAS Trial. Preprints 2019, 2019110389 (doi: 10.20944/preprints201911.0389.v1). Caicedo, D.; Devesa, P.; Alvarez, C.; Devesa, J. Why Should Growth Hormone (GH) Be Considered a Promising Therapeutic Agent for Arteriogenesis? Insights from the GHAS Trial. Preprints 2019, 2019110389 (doi: 10.20944/preprints201911.0389.v1).

Abstract

Despite the important role that the GH/IGF-I axis plays in vascular homeostasis, these kind of growth factors barely appear in articles addressing the neovascularization process. Currently, the vascular endothelium has turned to be considered as an authentic gland of internal secretion due to the wide variety of released factors and functions with local effect, including the paracrine/autocrine production of GH or IGF-I, for which the endothelium has specific receptors. In this comprehensive review, it will be described the evidence involving these proangiogenic hormones in arteriogenesis dealing with the arterial occlusion and making of them a potential therapy. It will be analyzed all those elements triggering the local and systemic production of GH/IGF-I and their possible role both in physiological and pathological conditions. The whole evidence will be combined with important data from the GHAS trial, in which GH or placebo were administrated to patients suffering from critical limb ischemia with no option for revascularization. We postulate that GH, alone or in combination, should be considered as a promising therapeutic agent for helping in the approach of the ischemic disease.

Subject Areas

GH and eNOS; IGF-I; oxidative stress and arterial inflammation; vascular homeostasis; Neovascularization; arteriogenesis; GHAS trial

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