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Chandrashekhar R. Gandhi, MSc, PhD

  • Professor, UC Department of Surgery



Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the United States and includes symptoms such as fatigue, abdominal pain, enlarged spleen, enlarged blood vessels and jaundice. The main characteristic of nonalcoholic fatty liver disease is an excessive amount of fat stored in liver cells. NAFLD progresses in some individuals to a more aggressive form known as Non-Alcoholic Steatohepatitis (NASH).

My research has two main areas of focus. First, my colleagues and I aim to elucidate the mechanisms of the initiation and progression of nonalcoholic fatty liver disease, which is a major challenge for adult and pediatric populations. In particular, we are looking at a mitochondrial protein augmenter of liver regeneration (ALR) deficiency, which forms an aggressive NASH in the animal model and humans, as discovered in my laboratory.

Second, my research aims to discover protocols for acute liver injury, which may be fatal, and establish endogenous factors that prevent the spread of liver fibrosis. My laboratory work focuses on determining whether blood protein ALR can be a biomarker for aggressive nonalcoholic fatty liver disease and whether genetic mutations or a decline of ALR may lead to disease progression.

I have a goal of figuring out whether ALR treatment could be useful in healing NAFLD. My research attempts to uncover how hepatic stellate cells direct acute liver failure independently. My colleagues and I accomplish this by modulating the resident cells’ functions and by infiltrating inflammatory and immune cells.

In my lab, we made a surprising discovery that an endotoxin (lipopolysaccharide, LPS) produced by gut bacteria, which is a highly inflammatory mediator, can reverse the phenotype of fibrogenic stellate cells to a non-fibrogenic physiological state. Our goal is to uncover non-inflammatory mimetics of LPS that can treat liver fibrosis.

At the beginning of my career, I was fascinated by the intercellular communication between different liver cell types that maintain their physiological function, which is essential for the health and function of other organs. The liver can accomplish this despite being exposed to a variety of different harmful agents. However, in certain scenarios, the liver becomes damaged itself, which leads to either acute failure or a progression to fibrosis, cirrhosis or cancer.

I have more than 40 years’ experience in my field, and I first joined the Cincinnati Children’s Hospital Medical team in 2012. Also, I was the first to discover that an endogenously produced potent vasoconstrictor endothelin-1 can be essential for liver fibrosis and portal hypertension and that endothelin inhibitors can be restorative.

My research has been funded by the American Heart Association, National Institutes of Health (NIH), the Veteran's Administration Merit grant and the Department of Defense. I have delivered lectures at numerous international institutions, have chaired and presented my work at several research symposia at international meetings and my research was highlighted at the 2015 Experimental Biology meeting.

MSc: Biochemistry, Nagpur University, India.

PhD: Biochemistry, Nagpur University, India.

Services and Specialties

Gastroenterology GI


Mechanisms of liver injury, immunological tolerance and steatohepatitis

Research Areas

Gastroenterology Hepatology and Nutrition, Fibrosis


CD14 is not required for carbon tetrachloride-induced hepatic inflammation and fibrosis with or without lipopolysaccharide challenge. Sharma, A; Wang, J; Gandhi, CR. Journal of Cellular Physiology. 2023; 238:1530-1541.

Stellate cell in hepatic inflammation and acute injury. Rani, R; Gandhi, CR. Journal of Cellular Physiology. 2023; 238:1226-1236.

Differential recruitment of monocyte-derived macrophages in control and stellate cell-depleted mice during recurrent carbon tetrachloride-induced acute liver injury. Sharma, A; Kudira, R; Wang, J; Miethke, A; Gandhi, CR. Journal of Cellular Physiology. 2022; 237:4215-4225.

Augmenter of liver regeneration: Mitochondrial function and steatohepatitis. Verma, AK; Sharma, A; Subramaniyam, N; Gandhi, CR. Journal of Hepatology. 2022; 77:1410-1421.

Endotoxin-Stimulated Hepatic Stellate Cells Augment Acetaminophen-Induced Hepatocyte Injury. Rani, R; Sharma, A; Wang, J; Kumar, S; Polaki, US; Gandhi, CR. The American journal of pathology. 2022; 192:518-535.

MRI Measures of Murine Liver Fibrosis. Lindquist, DM; Fugate, EM; Wang, J; Sharma, A; Gandhi, CR; Dillman, JR. Journal of Magnetic Resonance Imaging. 2021; 54:739-749.

Hepatic Steatosis in Infancy: The Beginning of Pediatric Nonalcoholic Fatty Liver Disease?. McNelis, K; Yodoshi, T; Divanovic, S; Gandhi, C; Kim, JH; Anton, CG; Trout, AT; Mouzaki, M. 2021; 2:e113.

Lipopolysaccharide Reverses Hepatic Stellate Cell Activation Through Modulation of cMyb, Small Mothers Against Decapentaplegic, and CCAAT/Enhancer-Binding Protein C/EBP Transcription Factors. Sharma, A; Verma, AK; Kofron, M; Kudira, R; Miethke, A; Wu, T; Wang, J; Gandhi, CR. Hepatology. 2020; 72:1800-1818.

Hepatic Deficiency of Augmenter of Liver Regeneration Predisposes to Nonalcoholic Steatohepatitis and Fibrosis. Kumar, S; Verma, AK; Rani, R; Sharma, A; Wang, J; Shah, SA; Behari, J; Salazar Gonzalez, R; Kohli, R; Gandhi, CR. Hepatology. 2020; 72:1586-1604.

Reply. Verma, AK; Gandhi, CR. Hepatology. 2020; 72:1157-1158.