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Updated: Jul 25, 2025

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Published on: March 7, 2022
Riboflavin protects against heart failure via SCAD-dependent DJ-1-Keap1-Nrf2 signalling pathway
Qingping Xu1,2, Yuhong Cao1,2, Xiaoyi Zhong1,2
1School of Chinese Materia Medica, Guangdong Pharmaceutical University, Guangzhou, China.
Riboflavin protects the heart in heart failure by boosting flavin adenine dinucleotide (FAD) and short-chain acyl-CoA dehydrogenase (SCAD) activity. This activates the DJ-1-Keap1-Nrf2 pathway, reducing oxidative stress and cell death.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Biochemistry
Background:
- Flavin adenine dinucleotide (FAD) demonstrates cardiovascular protective effects through short-chain acyl-CoA dehydrogenase (SCAD) supplementation.
- The role of riboflavin, a FAD precursor, in mitigating heart failure requires further elucidation.
Purpose of the Study:
- To investigate if riboflavin can improve heart failure.
- To determine if riboflavin activates SCAD and the DJ-1-Keap1-Nrf2 signaling pathway for cardioprotection.
Main Methods:
- Utilized a mouse model of transverse aortic constriction (TAC)-induced heart failure.
- Assessed cardiac structure, function, energy metabolism, and apoptosis.
- Analyzed signaling proteins in vivo and in vitro using cell apoptosis models.
Main Results:
- Riboflavin treatment improved cardiac function, ameliorated fibrosis, and reduced apoptosis in TAC mice.
- In vitro studies showed riboflavin decreased reactive oxygen species (ROS) and cardiomyocyte apoptosis.
- Riboflavin restored FAD, SCAD activity, activated DJ-1, and modulated the Keap1-Nrf2/HO1 pathway.
Conclusions:
- Riboflavin exerts cardioprotective effects against heart failure.
- Mechanism involves FAD-mediated stimulation of SCAD, activating the DJ-1-Keap1-Nrf2 pathway.
- This pathway improves oxidative stress and reduces cardiomyocyte apoptosis.
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