Potential Treatments for Reactive Oxygen Damage in the Kidneys

This video briefly runs over the significance of Post Myocardial Infarction Acute Kidney Injury and elaborates on the effect of deferoxamine and ferrostatin-1, at different concentrations, on the reduction of reactive oxygen species (ROS) and the lack of a synergistic effect if deferoxamine and ferrostatin-1 are treated together.

The story of me walking along the mystical paths of biomedical research has its roots in the 9th grade. Interested in cardiological research, I took my first step of faith by starting research at the Jiang Tian lab in October of 2018. At the Tian lab, I spent over a year grasping the experimental techniques of cell culture, genotyping PCR, and gel electrophoresis. In the beginning of my junior year, I searched for a research project matching my interests, and discovering a research project pertinent to diabetics with heart conditions, I was instantly hooked. My grandmother, whom I adore, has both of these conditions and the reality of millions of people like my grandmother potentially suffering from post-Myocardial infarction acute kidney injury compelled me to study this subject. Spending six months at the Gupta lab on this project, I was finally able to get tangible results! I proclaimed these results to the scientific community at the district science day, the state science day, and finally at the American Junior Academy of Science!

In the PDF attached, you can find an in-depth research paper to explain the rationale, methodology, data analysis, and conclusions. If interested, feel free to read it!

This poster outlines the scientific reasoning for the existence of post-Myocardial infarction acute kidney injury for diabetic patients. Furthermore, the mechanisms for deferoxamine (DFO) and ferrostatin-1 (Fer-1) to reduce reactive oxygen species (ROS) in order to attenuate acute kidney injury is also outlined. Lastly, the results illustrating the dose-dependent nature of DFO and Fer-1's reduction of ROS as well as the limitations is also found on this billboard.

Within this research presentation, I briefly discuss how the onset of a myocardial infarction for diabetic patient can potentially lead to acute kidney injury through the process of ROS formation. Furthermore, I discuss the biochemical mechanisms through which deferoxamine and ferrostatin-1 treatments reduce ROS and potentially attenuate acute kidney injury. Towards the final half of the presentation, the methodology employed to test the treatments of deferoxamine and ferrostatin-1 is explained. In the results and discussion sections, the dose-dependent reduction of ROS for increased concentrations of deferoxamine and ferrostatin-1 are shown and explained as well as the limitations of both treatments.