Japanese researchers are making groundbreaking discoveries on the mechanisms of aging and working to apply them. As we age, senescent cells, or aged cells that have stopped dividing, accumulate, causing inflammation that can damage blood vessels and organs. Animal experiments have shown that removing these cells improves kidney function and reduces arteriosclerosis. They have led to the identification of a drug and development of a vaccine to eliminate the cells.

Disrupted sleep-wake and molecular circadian rhythms are a feature of aging associated with metabolic disease and reduced levels of NAD⁺, yet whether changes in nucleotide metabolism control circadian behavioral and genomic rhythms remains unknown. Here, we reveal that supplementation with the NAD ⁺ precursor nicotinamide riboside (NR) markedly reprograms metabolic and stress-response pathways that decline with aging through inhibition of the clock repressor PER2. NR enhances BMAL1 chromatin binding genome-wide through PER2 ^K680 deacetylation, which in turn primes PER2 phosphorylation within a domain that controls nuclear transport and stability and that is mutated in human advanced sleep phase syndrome.

Scientists created a stem cell-based method to produce high-quality mitochondria at scale, enabling effective treatments for osteoarthritis and other diseases linked to mitochondrial dysfunction. Scientists have developed a groundbreaking method to mass-produce high-quality human mitochondria, a

Professor Kenji Osafune (Department of Cell Growth and Differentiation) and his team of researchers have devised an effective means to grow iPS cell-derived kidney progenitor cells, paving the way for renal regenerative therapies to become a reality. The findings are published in the journal Science Translational Medicine.

Modern medicine continues to be hampered by the lack of effective treatments for acute kidney injury (AKI) and chronic kidney disease (CKD). Regenerative medicine, such as cell replacement therapies, represents a new hope for patients. Yet, such therapeutic approaches require large-scale production of the necessary cells, which had remained a challenge until this discovery.

Using a mouse model of AKI, the research team first demonstrated the therapeutic potential of human iPS cell-derived nephron progenitor cells (hiPSC-NPCs). When these cells were transplanted into the kidneys of AKI mouse models induced by an anti-cancer drug, cisplatin, the animals’ survival was vastly improved by preventing the deterioration of kidney function.