Nicotinamide Riboside Protects Against Doxorubicin Cardiotoxicity: Preclinical Findings

Synopsis

In human iPSC-derived cardiomyocytes, nicotinamide riboside (NR) improved mitochondrial fusion, enhanced oxidative phosphorylation and ATP production, and upregulated ERRα, a key metabolic regulator. Blocking SIRT1 abolished these benefits, whereas activating SIRT1 boosted mitochondrial energetics through SIRT1–ERRα interaction. Under doxorubicin-induced cardiotoxicity, NR reduced oxidative stress, preserved mitochondrial function, and prevented apoptosis via the SIRT1/ERRα pathway. These results show that NR strengthens cardiac energetics in both healthy and stressed cells and support its potential for clinical use to protect the heart during chemotherapy.

Journal

Life Sciences