Connor Quinn

ORCID: 0009-0005-6916-5641
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About
Contact & Profiles
Research Areas
  • Liver Disease Diagnosis and Treatment
  • Diet, Metabolism, and Disease
  • Folate and B Vitamins Research
  • Liver physiology and pathology
  • Liver Disease and Transplantation
  • Diet and metabolism studies
  • Liver Diseases and Immunity
  • Adipose Tissue and Metabolism

Temple University
2021-2024

Nonalcoholic fatty liver disease (NAFLD) is the number one cause of chronic worldwide, with 25% these patients developing nonalcoholic steatohepatitis (NASH). NASH significantly increases risk cirrhosis and decompensated failure. Past studies in rodent models have shown that glycine-N-methyltransferase (GNMT) knockout results rapid steatosis, fibrosis, hepatocellular carcinoma progression. However, attenuation GNMT subjects molecular basis for its impact on process still unclear. To address...

10.3390/ijms23041986 article EN International Journal of Molecular Sciences 2022-02-11

Hepatic fibrosis is the primary determinant of mortality in patients with metabolic dysfunction–associated steatohepatitis (MASH). Transforming growth factor–β (TGFβ), a master profibrogenic cytokine, promising therapeutic target that has not yet been translated into an effective therapy part because liabilities associated systemic TGFβ antagonism. We have identified soluble folate receptor γ (FOLR3), which expressed humans but rodents, secreted protein elevated livers MASH those steatotic...

10.1126/scitranslmed.ade2966 article EN Science Translational Medicine 2023-09-27

Caloric restriction (CR) is known to enhance insulin sensitivity and reduce the risk of metabolic disorders; however, its molecular mechanisms are not fully understood. This study aims elucidate specific proteins pathways responsible for these benefits.

10.1002/oby.24150 article EN Obesity 2024-10-17

Abstract Non-alcoholic fatty liver disease (NAFLD) has become one of the most prominent forms chronic worldwide, mirroring obesity epidemic. NAFLD is number cause with 25% these patients developing nonalcoholic steatohepatitis (NASH). This significantly increases risk cirrhosis and decompensated failure. Past studies in rodent models have shown that knockout glycine- N -methyltransferase (GNMT) associated steatosis, fibrosis, hepatocellular carcinoma. However, attenuation GNMT subjects NASH...

10.1101/2021.12.03.470998 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-12-03

Abstract Hepatic fibrosis is the primary determinant of mortality in nonalcoholic steatohepatitis (NASH) patients. Antagonism transforming growth factor β (TGFβ), a master profibrogenic cytokine, promising therapeutic target that has not yet been translated into an effective therapy, due part to lack animal models resembling human phenotype NASH. Here we have identified soluble secreted folate receptor gamma (FOLR3), expressed humans but rodents, protein elevated livers NASH subjects with...

10.1101/2022.07.21.500829 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2022-07-22
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