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Kuo Du

Adjunct Assistant Professor in the Department of Medicine
Medicine, Gastroenterology

Scholarly Works - Conferences


Targeting YAP-mediated HSC death susceptibility and senescence for treatment of liver fibrosis.

Conference Hepatology · June 1, 2023 BACKGROUND AND AIMS: Liver fibrosis results from the accumulation of myofibroblasts (MFs) derived from quiescent HSCs, and yes-associated protein (YAP) controls this state transition. Although fibrosis is also influenced by HSC death and senescence, whethe ... Full text Open Access Link to item Cite

Hepatocyte Smoothened Activity Controls Susceptibility to Insulin Resistance and Nonalcoholic Fatty Liver Disease.

Conference Cell Mol Gastroenterol Hepatol · 2023 BACKGROUND & AIMS: Nonalcoholic steatohepatitis (NASH), a leading cause of cirrhosis, strongly associates with the metabolic syndrome, an insulin-resistant proinflammatory state that disrupts energy balance and promotes progressive liver degeneration. We a ... Full text Link to item Cite

Aging reduces liver resiliency by dysregulating Hedgehog signaling.

Conference Aging Cell · February 2022 Older age is a major risk factor for damage to many tissues, including liver. Aging undermines resiliency and impairs liver regeneration. The mechanisms whereby aging reduces resiliency are poorly understood. Hedgehog is a signaling pathway with critical m ... Full text Link to item Cite

Inhibiting xCT/SLC7A11 induces ferroptosis of myofibroblastic hepatic stellate cells and protects against liver fibrosis

Conference · 2019 Background and Aims Liver fibrosis develops in the context of excessive oxidative stress, cell death and accumulation of myofibroblasts (MFs) derived from hepatic stellate cells (HSCs). Ferroptosis is a type of regulated cell death that can be ca ... Full text Cite

Hedgehog-YAP Signaling Pathway Regulates Glutaminolysis to Control Activation of Hepatic Stellate Cells.

Conference Gastroenterology · April 2018 BACKGROUND & AIMS: Cirrhosis results from accumulation of myofibroblasts derived from quiescent hepatic stellate cells (Q-HSCs); it regresses when myofibroblastic HSCs are depleted. Hedgehog signaling promotes transdifferentiation of HSCs by activating Yes ... Full text Link to item Cite