Brian N. Finck

This study identifies Dipyridamole as a drug that rescues mitochondrial dysfunction and neuronal death in ALS and AD iPSC-derived neurons by enhancing mitochondrial pyruvate uptake.

This study identifies a preoptic neuronal population that regulates energy expenditure and balance through daily activity patterns and metabolic responses.

This study identifies GPT2-dependent alanine catabolism as a metabolic vulnerability in MYC-driven liver cancer, showing that inhibiting GPT2 reduces tumor growth in mouse models.

This study shows a Western high-phosphate diet worsens CKD-MBD features in Alport Syndrome mice, increasing PTH and FGF23 while reducing klotho, but does not induce vascular calcification.

This paper shows that deleting MondoA globally protects against diet-induced obesity by increasing energy expenditure through enhanced glucose uptake and glycolytic flux, leading to elevated glycerol synthesis and lipolysis.

This study shows that overexpressing NAMPT in adipocytes protects against metabolic dysfunction in male obese mice but not females, via improved interorgan communication and extracellular vesicle effects.

This study shows that inducing TFEB in Kupffer cells reduces cell death, lipid accumulation, and inflammation in MASLD.

The paper shows that hematopoietic progenitors adjust to metabolic perturbations intrinsically to maintain homeostasis, independent of feedback from mature cells.

This study identifies Site-1 Protease (S1P) as a negative regulator of muscle mass and mitochondrial metabolism by controlling the TGF-β target gene MSS51.

This paper identifies BIOIO-1001 as a dual mTOR/NAD+ acting gerotherapy that reduces metabolic derangements, inflammation, and fibrosis in NASH and ALS models.

This study shows that Mogat1 is important for adipocyte differentiation in vitro but not for adiposity or metabolic outcomes in mice on a high-fat diet.