A hypothesis concerning the role of PPAR family on cardiac energetics in Adriamycin‐induced cardiomyopathy
Molecular Docking Simulation
PPAR gamma
0303 health sciences
03 medical and health sciences
Doxorubicin
Iron
Humans
Myocytes, Cardiac
Cardiomyopathies
Heme Oxygenase-1
Sulfur
3. Good health
DOI:
10.1002/jat.4374
Publication Date:
2022-08-10T00:28:00Z
AUTHORS (4)
ABSTRACT
Adriamycin is an effective anti-neoplastic drug against a variety of cancer types. However, the causes adverse side effects in number organ systems. Cardiomyopathy one life-threatening Adriamycin. In current work, we have derived hypothesis with possible involvement PPAR family members development Adriamycin-induced cardiomyopathy. Dysregulation by impairment transport and β-oxidation fatty acids, key substrate for ATP synthesis heart. Evidences suggest that dysregulation alters recruitment glucose transporters. Furthermore, heme oxygenase-1 crucial enzyme regulating iron homeostasis heart whose expression regulated family. Inverse relationship exists between levels PPARγ oxygenase-1. upregulates which turn disrupts cardiomyocytes. Our molecular docking results show has high affinity iron-binding sites oxygenase-1, thereby hindering formation iron-sulfur complex. The lack complex impairs electron chain. addition, succinate dehydrogenase subunit A downregulated this uncouples Krebs cycle from ETC. Further, increases concentration succinate, further mitochondrial membrane potential. Overall, present hypothesize alteration major metabolic chaos oxidative stress caused during
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