As of 2014, there are approximately 14.5 million cancer survivors within the United States and this populationis projected to grow to 19 million by 2024. Cancer survivors exhibit an accelerated aging phenotype that ishypothesized to be a result of their exposure to chemotherapy. Despite the preponderance of evidencesuggesting that this accelerated aging phenotype happens, there are few basic science initiatives poised tostudy the underlying molecular mechanisms and their therapeutic implications.

Lens, an avascular organ, relies heavily on a network of transporting systems to deliver nutrients and otheressential components to bulky lens fibers and excrete wastes. Differentiated nuclear fiber cells never turn overand oxidative stress is a major cause of age related cataracts. Connexin (Cx)-forming gap junction channelsplay an essential role for the metabolic homeostasis of the lens. Besides gap junctions, connexins formhemichannels, permitting transport of molecules between the cell and its extracellular environment.

The consumption of 3 fatty acid-rich foods is associated with multiple health benefits, including theprevention of cardiovascular and neurologic diseases. However, while the dietary consumption of these fattyacids often shows benefits, the use of fish-oil containing capsules and other supplements to augment theintake of ?-3 fatty acids has produced largely negative results on these health outcomes in clinical trials.

Acute kidney injury (AKI) and chronic kidney disease (CKD) are major contributors to overall morbidity andmortality in patients in the US. The overall objective of the proposed study is to establish untargeted andtargeted spatial metabolomics analysis of tissues from normal and diseased kidneys to assess cellularmetabolic states associated with healthy function, acute injury, chronic condition, and recovery.

Cellular senescence causes inflammation, oxidative stress, and mitochondrial dysfunction, which have been implicated in the pathogenesis of age-related diseases. Accordingly, genetic depletion of senescent cells has recently been shown to extend lifespan and attenuate aging-related diseases. However, the cellular mechanisms underlying senescence and how it may promote diseases of aging are unclear. Recent work from my laboratory has implicated a role for ALCAT1 in linking cellular senescence with aging-related diseases.

As of 2014, there are approximately 14.5 million cancer survivors within the United States and this populationis projected to grow to 19 million by 2024. Cancer survivors exhibit an accelerated aging phenotype that ishypothesized to be a result of their exposure to chemotherapy. Despite the preponderance of evidencesuggesting that this accelerated aging phenotype happens, there are few basic science initiatives poised tostudy the underlying molecular mechanisms and their therapeutic implications.