NIH R01 · 2025
Impaired VLDL secretion in progression of NAFLD and NASH in mice and humans
PROJECT SUMMARY/ABSTRACT The major OBJECTIVES in this application are to expand understanding of mediators of fibrogenic injury and HCC development associated with impaired VLDL secretion in both mice and humans. Our proposal is SIGNIFICANT because of the unmet need to identify subsets of patients with NAFLD whose disease will progress and where a more tailored approach might inform therapeutic strategies for prevention and reversal of NASH/fibrosis and the development of HCC. The BACKGROUND is that genetic defects (APOB, MTTP, TM6SF2) that impair hepatic VLDL secretion cause hepatic steatosis and progress to NASH with fibrosis and HCC, even without obesity or insulin resistance. In…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.