Area of research
Epidemiology · Pathology and Forensic Medicine
Research interest
Research interests include Endocrinology, Internal medicine, Lipotoxicity, Autophagy, AMPK, and Oxidative stress.
Hepatic NMNAT1 is required to defend against alcohol-associated fatty liver disease
The gut microbiota reprograms intestinal lipid metabolism through long noncoding RNA <i>Snhg9</i>
Gut-derived ammonia contributes to alcohol-related fatty liver development via facilitating ethanol metabolism and provoking ATF4-dependent de novo lipogenesis activation
mTORC1 inhibition uncouples lipolysis and thermogenesis in white adipose tissue to contribute to alcoholic liver disease
Inhibition of STAT3 signaling contributes to the anti-melanoma effects of chrysoeriol
Activation of AMP-Activated Protein Kinase-Sirtuin 1 Pathway Contributes to Salvianolic Acid A-Induced Browning of White Adipose Tissue in High-Fat Diet Fed Male Mice
Salidroside alleviates lipotoxicity-induced cell death through inhibition of TLR4/MAPKs pathway, and independently of AMPK and autophagy in AML-12 mouse hepatocytes
Glutathione disulfide sensitizes hepatocytes to TNFα-mediated cytotoxicity via IKK-β S-glutathionylation: a potential mechanism underlying non-alcoholic fatty liver disease
The <scp>TLR</scp>4‐<scp>IRE</scp>1α pathway activation contributes to palmitate‐elicited lipotoxicity in hepatocytes
Sirtuin 3 acts as a negative regulator of autophagy dictating hepatocyte susceptibility to lipotoxicity
Nicotinamide protects hepatocytes against palmitate-induced lipotoxicity via SIRT1-dependent autophagy induction
Nicotinamide ameliorates palmitate-induced ER stress in hepatocytes via cAMP/PKA/CREB pathway-dependent Sirt1 upregulation
Rectification of impaired adipose tissue methylation status and lipolytic response contributes to hepatoprotective effect of betaine in a mouse model of alcoholic liver disease
Nuclear factor (erythroid-derived 2)-like 2 activation-induced hepatic very-low-density lipoprotein receptor overexpression in response to oxidative stress contributes to alcoholic liver disease in mice
Protection of nicotinic acid against oxidative stress-induced cell death in hepatocytes contributes to its beneficial effect on alcohol-induced liver injury in mice
Inhibition of ERK1/2 pathway suppresses adiponectin secretion via accelerating protein degradation by Ubiquitin–proteasome system: Relevance to obesity-related adiponectin decline