7-days of FREE Audio papers, translation & more with Prime
7-days of FREE Prime access
7-days of FREE Audio papers, translation & more with Prime
7-days of FREE Prime access
https://doi.org/10.54097/hset.v19i.2661
Copy DOIPublication Date: Nov 17, 2022 | |
Citations: 1 | License type: CC BY-NC 4.0 |
While exhibiting great value in treating multiple cancers, the chemotherapy drug, Doxorubicin, also manifests many side effects that significantly affect the post-chemotherapy life of patients. In the cardiac system, Doxorubicin causes oxidative stress due to increasing amount of Reactive oxygen species (ROS), and it promotes production of inflammatory cytokines. Oxidative stress and inflammatory cytokines then activate p38 mitogen-activated protein kinase (p38 MAPK), which can stimulate cardiomyocyte apoptosis. In the nervous system, Doxorubicin activates both extracellular signal-regulated kinase (ERK) and p38 MAPK. p38 MAPK predominately determines the result, leading to an overall reduction in Long-term Potentiation (LTP), or an analogous process of Long-term Facilitation (LTF). Moreover, neuroinflammatory effect achieved through the p38 MAPK pathway contributes to memory deficits by killing neurons excessively. Various inhibitors of p38 MAPK have shown promising results in lessening the effects of p38 MAPK, indicating future possibilities of using those inhibitors to ensure a safer application of Doxorubicin, while preserving the pharmacological values and properties of Doxorubicin.
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.