Senthil Kumar Venugopal
Professor & Dean
Faculty of Life Sciences and Biotechnology (FLSB)

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Profile

PROFESSIONAL EXPERIENCE:

Associate Professor: South Asian University, New Delhi (2011-till date)
Ramalingaswami Fellow: Institute of Liver and Biliary Sciences, New Delhi (2009-2011)
Assistant Professor: University of California Davis Medical Center, Sacramento, CA, USA (2006-2009)
Post Graduate Researcher: University of California Davis Medical Center, Sacramento, CA, USA (2002-2006)
Post-Doctoral Fellow: UT Southwestern Medical Center, Dallas, TX, USA (2001-2002)

RESEARCH INTERESTS:

The liver is a multifunctional organ performing metabolism, biosynthesis, excretion, secretion and detoxification. During this process, it can be damaged by several toxins such as alcohol, fatty food, viral infection, etc., and in response to that the liver can be regenerated. If the cell loss exceeds the proliferation, then chronic liver injury occurs. This leads to impaired regeneration, which is one of the key features of most liver disorders. However, unlike any other organ, the liver can regenerate by cell proliferation following either partial hepatectomy or hepatic injury. Depending on the extent of injury, the balance shifts from regeneration to cellular loss and hepatic failure. In case of alcoholic and non-alcoholic injuries, the liver accumulates lot of fat and becomes fatty liver. Continued storage results in the steatohepatitis, where oxidative stress and inflammation accelerate the liver injury process. Stellate cells get activated and liver become fibrotic, leading to cirrhosis and sometimes to liver cancer. Hepatic viruses such as hepatitis B virus (HBV) and hepatitis C virus also can lead to the chronic liver injury leading to liver cancer. All these processes are tightly controlled by the expression of various genes. Currently, my laboratory is working on the, a) role of hepatitis B virus in chronic liver disease; b) role of butyrate in modulating the cell viability of hepatic cancer cells; c) molecular mechanisms involved in regulating liver regeneration; and d) role of glucose homeostasis in non-alcoholic fatty liver disease.

Qualifications

  • PhD in Biochemistry from All India Institute of Medical Sciences, New Delhi , in 2000
  • M.Tech. in Biotechnology from Jadavpur University, Calcutta , in 1995

Awards & Honours

  • Ramalingaswamy Fellowship by Department of Biotechnology, India at India, in 2009-2014
  • Member, American Association for the Study of the Liver Diseases

Recent Publications

  • Gupta P, Venugopal SK. Augmenter of liver regeneration: A key protein in liver regeneration and pathophysiology. Hepatol Res. 2018 Apr 6.

  • Singh AK, Rooge SB, Varshney A, Vasudevan M, Bhardwaj A, Venugopal SK, Trehanpati N, Kumar M, Geffers R, Kumar V, Sarin SK. Global micro RNA expression profiling in the liver biopsies of Hepatitis B Virus infected patients suggests specific miRNA signatures for viral persistence and hepatocellular injury. Hepatology. 2018; 67: 1695-1709.

  • Venugopal SK, Jialal I. Biochemistry, Low density lipoprotein. StatPearls Publishing. 2018 Jan-2018 Apr 23.

  • Pant K, Misra AK, Venugopal SK. MicroRNAs in the progression of hepatocellular carcinoma. In MicroRNA: Prospectives in Health and Diseases. Ed. Paul J. Publisher: CRC Press. Taylor & Francis Group. 2018; 141-172.

  • Dhole B, Gupta S, Venugopal SK, Kumar A. Triiodothyronine stimulates VEGF expression and secretion via steroids and HIF-1a in murine Leydig cells. Systems Biol Reprod Med. 2018; 64:191-201.

  • Pant K, Yadav AK, Gupta P, Islam R, Jain A, Saraya AN, Venugopal SK. Butyrate induces ROS-mediated apoptosis via modulation of miRNA-22/SIRT-1 regulatory axis in Hepatoma cells. Redox Biol. 2017; 12:340-349.

  • Pant K, Saraya AN, Venugopal SK. Oxidative stress plays a key role in butyrate-mediated autophagy via Akt/mTOR pathway in hepatoma cells. Chem Biol. Interactions. 2017;  273:99-106.

  • Pant K and Venugopal SK. Circulating microRNAs: Possible role as non-invasive diagnostic biomarkers in Liver diseases. Clin Res in Hepatol and Gastro. 2017; 41: 370-377.

  • Pant K, Yadav AK, Gupta P, Rathore AS, Naik B, Venugopal SK. Humic acid inhibits HBV-induced autophagosome formation and induces apoptosis in HBV-transfected Hep G2 cells. Scientific Reports. 2016;6:34496.

  • Pant K, Gupta P, Damania P, Yadav AK, Gupta A, Ashraf A, Venugopal SK. Mineral pitch induces apoptosis and inhibits proliferation via modulating reactive oxygen species in hepatic cancer cells. BMC Complement Alternate Med. 2016;16(1):148.

  • Kumar S, Gupta P, Khanal S, Shahi A, Kumar P, Sarin SK, Venugopal SK. Hepatitis B Virus X protein induces autophagosome formation by inhibiting microRNA-30a via targetting beclin-1 in hepatic cells. FEBS J. 2015; Mar 282(6):1152-63.

  • Damania P, Sen B, Dar SB, Kumar S, Kumari A, Gupta E, Sarin SK, Venugopal SK. Hepatitis B virus induces cell proliferation via HBx-induced microRNA-21 in hepatocellular carcinoma by targeting programmed cell death protein4 (PDCD4) and phosphatase and tensin homologue (PTEN). PLOS one. 2014 Mar 14;9(3):e91745.

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