Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Faculty Publications Article Faculty Publications -Articles Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Creator An entity primarily responsible for making the resource Ramasamy, Sumathi; Jeyaram, Kanimozhi; Arunachalam, Sankarganesh; Sankar, Muthumanickam Title A name given to the resource Impact of Endothelial Cell Repair Mechanisms on Doxorubicin-Induced Cardiomyopathy: Exploring Molecular Docking and Simulation studies of Angiogenic Factors Date A point or period of time associated with an event in the lifecycle of the resource 01-01-2025 Source A related resource from which the described resource is derived Turkish Computational and Theoretical Chemistry;Volume;9;Issue;5;pp.138-156 Identifier An unambiguous reference to the resource within a given context <a href="https://doi.org/10.33435/tcandtc.1698973" target="_blank" rel="noreferrer noopener">https://doi.org/10.33435/tcandtc.1698973</a> <br /><br /><a href="https://www.scopus.com/pages/publications/105036357417?origin=resultslist" target="_blank" rel="noreferrer noopener">https://www.scopus.com/pages/publications/105036357417?origin=resultslist</a> Coverage The spatial or temporal topic of the resource, the spatial applicability of the resource, or the jurisdiction under which the resource is relevant Ramasamy S., Department of Biotechnology, Kalasalingam Academy of Research and Education, Krishnankoil, Virudhunagar, Tamilnadu, 626126, India; Jeyaram K., Department of Biotechnology, Kalasalingam Academy of Research and Education, Krishnankoil, Virudhunagar, Tamilnadu, 626126, India; Arunachalam S., Department of Life Sciences, Christ (Deemed to be) University, Karnataka, Bengaluru, 560029, India; Sankar M., Department of Bioinformatics, Alagappa University, Tamil Nadu, Karaikudi, 630001, India Description An account of the resource Doxorubicin (Dox), despite being an effective anti-cancer drug, also causes cytotoxicity to noncancerous tissues. ECs are highly abundant in the heart; thus, endothelial dysfunction is a major cause of doxorubicin-induced cardiomyopathy. The release of EPCs triggered by endothelial dysfunction, participates in the growth of new blood vessels and the repair of damaged endothelium to promote repair mechanism. The current study aimed to evaluate the effects of doxorubicin on SDF1/CXCR4 pathway via in silico molecular docking and simulation studies. Remarkably, heparin binding site of SDF1at LEU: 29 might be preoccupied by doxorubicin leads to poor expression because SDF1 activity heavily depends on its binding sites. On the other hand, active sites of CXCR4 at ASP: 171 and GLU: 288 also engaged by dox, leading to the assumption that doxorubicin restrict the receptor activity. Additionally, the interaction of doxorubicin at the proton acceptor site and ATP binding sites of VEGFR1, including ASP: 1022, GLY: 836, ALE: 837 and PHE: 838, suppresses the function of the receptor in the MAPK1/ERK2 and AKT1 signaling cascades. The co-expressing factor involved in SDF1/CXCR4 like VEGFR2, ANGPT1 and SHIP2 were also affected by specific amino acid interactions. This induces alterations in several vital biochemical pathways, leading to metabolic chaos. Taken together, it is hypothesize that doxorubicin-mediated functional inactivity of SDF1 via its receptor CXCR4 and VEGFR1 impaired the cardiac EPCs regulation on angiogenesis and vascularization. (2025), (DergiPark). All rights reserved. Subject The topic of the resource Angiogenesis; CXCR4; Doxorubicin; EPCs; SDF-1; vascularization Publisher An entity responsible for making the resource available DergiPark Relation A related resource ISSN: 25871722; Language A language of the resource English Type The nature or genre of the resource Article Rights Information about rights held in and over the resource All Open Access; Gold Open Access Format The file format, physical medium, or dimensions of the resource online