TY - JOUR
T1 - Literature-based enrichment insights into redox control of vascular biology
AU - Essack, Magbubah
AU - Salhi, Adil
AU - Stanimirovic, Julijana
AU - Tifratene, Faroug
AU - Raies, Arwa Bin
AU - Hungler, Arnaud
AU - Uludag, Mahmut
AU - Van Neste, Christophe
AU - Trpkovic, Andreja
AU - Bajic, Vladan P.
AU - Bajic, Vladimir B.
AU - Isenovic, Esma R.
N1 - Publisher Copyright:
© 2019 Magbubah Essack et al.
PY - 2019
Y1 - 2019
N2 - In cellular physiology and signaling, reactive oxygen species (ROS) play one of the most critical roles. ROS overproduction leads to cellular oxidative stress. This may lead to an irrecoverable imbalance of redox (oxidation-reduction reaction) function that deregulates redox homeostasis, which itself could lead to several diseases including neurodegenerative disease, cardiovascular disease, and cancers. In this study, we focus on the redox effects related to vascular systems in mammals. To support research in this domain, we developed an online knowledge base, DES-RedoxVasc, which enables exploration of information contained in the biomedical scientific literature. The DES-RedoxVasc system analyzed 233399 documents consisting of PubMed abstracts and PubMed Central full-text articles related to different aspects of redox biology in vascular systems. It allows researchers to explore enriched concepts from 28 curated thematic dictionaries, as well as literature-derived potential associations of pairs of such enriched concepts, where associations themselves are statistically enriched. For example, the system allows exploration of associations of pathways, diseases, mutations, genes/proteins, miRNAs, long ncRNAs, toxins, drugs, biological processes, molecular functions, etc. that allow for insights about different aspects of redox effects and control of processes related to the vascular system. Moreover, we deliver case studies about some existing or possibly novel knowledge regarding redox of vascular biology demonstrating the usefulness of DES-RedoxVasc. DES-RedoxVasc is the first compiled knowledge base using text mining for the exploration of this topic.
AB - In cellular physiology and signaling, reactive oxygen species (ROS) play one of the most critical roles. ROS overproduction leads to cellular oxidative stress. This may lead to an irrecoverable imbalance of redox (oxidation-reduction reaction) function that deregulates redox homeostasis, which itself could lead to several diseases including neurodegenerative disease, cardiovascular disease, and cancers. In this study, we focus on the redox effects related to vascular systems in mammals. To support research in this domain, we developed an online knowledge base, DES-RedoxVasc, which enables exploration of information contained in the biomedical scientific literature. The DES-RedoxVasc system analyzed 233399 documents consisting of PubMed abstracts and PubMed Central full-text articles related to different aspects of redox biology in vascular systems. It allows researchers to explore enriched concepts from 28 curated thematic dictionaries, as well as literature-derived potential associations of pairs of such enriched concepts, where associations themselves are statistically enriched. For example, the system allows exploration of associations of pathways, diseases, mutations, genes/proteins, miRNAs, long ncRNAs, toxins, drugs, biological processes, molecular functions, etc. that allow for insights about different aspects of redox effects and control of processes related to the vascular system. Moreover, we deliver case studies about some existing or possibly novel knowledge regarding redox of vascular biology demonstrating the usefulness of DES-RedoxVasc. DES-RedoxVasc is the first compiled knowledge base using text mining for the exploration of this topic.
UR - http://www.scopus.com/inward/record.url?scp=85068493861&partnerID=8YFLogxK
U2 - 10.1155/2019/1769437
DO - 10.1155/2019/1769437
M3 - Review article
C2 - 31223421
AN - SCOPUS:85068493861
SN - 1942-0900
VL - 2019
JO - Oxidative medicine and cellular longevity
JF - Oxidative medicine and cellular longevity
M1 - 1769437
ER -