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ROS and diseases: role in metabolism and energy supply

Molecular and cellular biochemistry, 2020-04, Vol.467 (1-2), p.1-12 [Peer Reviewed Journal]

Springer Science+Business Media, LLC, part of Springer Nature 2019 ;COPYRIGHT 2020 Springer ;Molecular and Cellular Biochemistry is a copyright of Springer, (2019). All Rights Reserved. ;ISSN: 0300-8177 ;EISSN: 1573-4919 ;DOI: 10.1007/s11010-019-03667-9 ;PMID: 31813106

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  • Title:
    ROS and diseases: role in metabolism and energy supply
  • Author: Yang, Shenshu ; Lian, Gaojian
  • Subjects: Biochemistry ; Biomedical and Life Sciences ; Cardiology ; Diseases ; Energy metabolism ; Life Sciences ; Medical Biochemistry ; Metabolism ; Oncology ; Reactive oxygen species ; Researchers
  • Is Part Of: Molecular and cellular biochemistry, 2020-04, Vol.467 (1-2), p.1-12
  • Description: Researches dedicated to reactive oxygen species (ROS) had been performed for decades, yet the outcomes remain controversial. With the relentless effort of studies, researchers have explored the role of ROS in biosystem and various diseases. ROS are beneficial for biosystem presenting as signalling molecules and enhancing immunologic defence. However, they also have harmful effects such as causing tissue and organ damages. The results are controversial in studies focusing on ROS and ROS-related diseases by regulating ROS with inhibitors or promotors. These competing results hindered the process for further investigation of the specific mechanisms lying behind. The opinions presented in this review interpret the researches of ROS from a different dimension that might explain the competing results of ROS introduced so far from a broader perspective. This review brings a different thinking to researchers, with the neglected features and potentials of ROS, to relate their works with ROS and to explore the mechanisms between their subject and ROS.
  • Publisher: New York: Springer US
  • Language: English
  • Identifier: ISSN: 0300-8177
    EISSN: 1573-4919
    DOI: 10.1007/s11010-019-03667-9
    PMID: 31813106
  • Source: AUTh Library subscriptions: ProQuest Central
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