Nicotinamide mononucleotide (NMN) reduces heart scarring to restore the blood-pumping organ’s size and thickness in mice.
Heart scar tissue accumulation (cardiac fibrosis) is a significant contributor to heart failure by increasing the stiffness of heart cavities and diminishing blood pumping capacity. Finding ways to inhibit this process can improve heart function. Research has found that treatment with nicotinamide mononucleotide (NMN), a precursor to an essential bioenergetic molecule in all cells, can mitigate scar tissue buildup in the kidney and liver. However, whether this applies to the human heart remains open for investigation.
Liu and colleagues from Central South University in China published a study in Life Sciences indicating that injecting mice with 500 mg/kg of NMN every three days improved heart dysfunction, reduced scar tissue accumulation, and diminished heart organ enlargement in mice with chemically induced cardiac fibrosis. The China-based research team also uncovered pathway-related details for how NMN provides these effects in cardiac fibrosis. Findings from the study suggest NMN helps slow cardiac fibrosis progression to prevent heart disease onset and provide pathway insight for developing other therapeutics for heart dysfunction from fibrosis.