Stimulating a longevity-linked protein with nicotinamide mononucleotide (NMN) reduces tissue scarring progression and subsequent kidney disease.
When our kidneys become diseased, they undergo irreversible changes in function and overall structure that progress over months and years. Tissue scarring, or what’s called fibrosis in the medical field, contributes substantially to the advancement of kidney disease. We currently lack treatment options to delay and prevent kidney disease complications and progression from tissue scarring. So, understanding how tissue scarring progresses has become urgent for developing better therapeutic options.
Huang and colleagues from Nantong University in China published a study in Cell Death Discovery indicating that stimulating a protein linked to anti-aging that is involved in metabolism called sirtuin1 (SIRT1) attenuates kidney scarring progression in mice. After causing kidney damage, the research team saw that boosting levels of nicotinamide adenine dinucleotide (NAD+), a factor essential for SIRT1 activity, diminished tissue scarring markers. These findings provide some illumination for the cellular mechanisms by which tissue scarring accumulates to facilitate kidney damage, which may help with the development of therapeutic options to slow age-related kidney disease.