Preprint Review Version 1 This version is not peer-reviewed

Pathophysiological Aspects of Vascular Remodeling in Cardiopulmonary Lesions: Influence of ID3 & Estrogenic Endocrine Disruptors

Version 1 : Received: 18 July 2018 / Approved: 19 July 2018 / Online: 19 July 2018 (12:57:32 CEST)

How to cite: Avecilla, V.; Doke, M. Pathophysiological Aspects of Vascular Remodeling in Cardiopulmonary Lesions: Influence of ID3 & Estrogenic Endocrine Disruptors. Preprints 2018, 2018070334 (doi: 10.20944/preprints201807.0334.v1). Avecilla, V.; Doke, M. Pathophysiological Aspects of Vascular Remodeling in Cardiopulmonary Lesions: Influence of ID3 & Estrogenic Endocrine Disruptors. Preprints 2018, 2018070334 (doi: 10.20944/preprints201807.0334.v1).

Abstract

Cardiopulmonary lesions, which manifest from various types of diseases such as pulmonary arterial hypertension, atherosclerosis, pulmonary arteriovenous malformations, lymphangioleiomyomatosis, and peripheral arterial disease, pose a public health problem. Vascular remodeling, which refers to alternations to the structure of the vessel is an important pathophysiological feature of these diseases. The Inhibitor of DNA-binding/Differentiation-3 (ID3), which is part of the ID family of transcriptional regulators, has been demonstrated to contribute to an essential role in the vasculature and therefore may influence the alterations of these lesions. This review will cover the existing understanding of how ID3 may contribute to cardiopulmonary lesion perturbations via involvement in vascular remodeling. Furthermore, based on the accumulative quantity of reports that indicate oxidative stress plays a essential function in the pathophysiology of vascular remodeling, we will also consider the impact of exposure to estrogenic endocrine disruptors (EEDs) such as polychlorinated biphenyls (PCBs) and bisphenol A (BPA) on ID3 & cardiopulmonary disease. Improved understanding of how ID3 pathways contributes to these molecular mechanisms in the lesion will prospectively deliver beneficial information in the mediation of vascular remodeling associated with ID3 & EED exposure, which may play an essential role in cardiopulmonary disease prevalence.

Subject Areas

cardiopulmonary lesions, endocrine disruptors, ID3, vascular dysfunction, vascular remodeling

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