Finkel In the News
NHLBI's Dr. Toren Finkel joined a live radio panel discussion on the Diane Rehm Show to discuss his anti-aging research involving work on mice. Other panel members included National Institute on Aging's Dr. Mark Mattson and Massachusetts Institute of Technology's Leonard Guarente.
NHLBI intramural investigators Toren Finkel and Herbert Geller were among the 388 newly-elected AAAS Fellows who were recognized by their peers for their efforts to advance science or its applications. The new AAAS Fellows will be honored at the AAAS Fellows Forum on Saturday, 15 February during the AAAS Annual Meeting in Chicago, where they will receive a certificate and a blue and gold rosette as a symbol of their distinguished accomplishments
By lowering the expression of a single gene, researchers at the National Institutes of Health have extended the average lifespan of a group of mice by about 20 percent -- the equivalent of raising the average human lifespan by 16 years, from 79 to 95. The research team targeted a gene called mTOR, which is involved in metabolism and energy balance, and may be connected with the increased lifespan associated with caloric restriction.
In a paper just published in Cell Reports, J. Julie Wu and colleagues from Toren Finkel’s group at the NHLBI use a hypomorphic allele of mTor to probe the effects of reduced mTor expression in mice. They found that reduced mTOR did lead to a significant increase in lifespan, but age-related improvements varied from tissue to tissue.
Recent years have witnessed a growing excitement in the field of mitochondrial biology with a dramatic increase in our appreciation of the diversity and complexity of mitochondrial function. Rather than simply acting as isolated energy-generating organelles, as once thought, we now know that these organelles form a dynamic network that is subject to continuous remodeling and is integrated into cellular signaling pathways.
Although initially viewed as unregulated, increasing evidence suggests that cellular necrosis often proceeds through a specific molecular program. In particular, death ligands such as tumour necrosis factor (TNF)-? activate necrosis by stimulating the formation of a complex containing receptor-interacting protein 1 (RIP1) and receptor-interacting protein 3 (RIP3). Relatively little is known regarding how this complex formation is regulated.