Transcriptome changes in stages of non-alcoholic fatty liver disease

doi:10.4254/wjh.v14.i7.1382

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World Journal of Hepatology

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Clinical and Translational Research

World J Hepatol. Jul 27, 2022; 14(7): 1382-1397
Published online Jul 27, 2022. doi: 10.4254/wjh.v14.i7.1382

Transcriptome changes in stages of non-alcoholic fatty liver disease

Jihad Aljabban, Michael Rohr, Saad Syed, Kamal Khorfan, Vincent Borkowski, Hisham Aljabban, Michael Segal, Mohamed Mukhtar, Mohammed Mohammed, Maryam Panahiazar, Dexter Hadley, Ryan Spengler, Erin Spengler

Jihad Aljabban, Vincent Borkowski, Michael Segal, Ryan Spengler, Department of Medicine, University of Wisconsin Hospital and Clinics, Madison, WI 53792, United States

Michael Rohr, Department of Medicine, University of Central Florida College of Medicine, Orlando, FL 32827, United States

Saad Syed, Department of Medicine, Northwestern Memorial Hospital, Chicago, IL 60611, United States

Kamal Khorfan, Department of Gastroenterology and Hepatology, University of California San Francisco-Fresno , Fresno, CA 93701, United States

Hisham Aljabban, Department of Medicine, Barry University, Miami, FL 33161, United States

Mohamed Mukhtar, Department of Medicine, Michigan State University College of Human Medicine, East Lansing, MI 49503, United States

Mohammed Mohammed, Department of Medicine, Windsor University School of Medicine, Saint Kitts 1621, Cayon, Saint Kitts and Nevis

Maryam Panahiazar, Department of Surgery, University of California San Francisco, San Francisco, CA 94305, United States

Dexter Hadley, Department of Artificial Intelligence, Pathology, University of Central Florida College of Medicine , Orlando, FL 32827, United States

Erin Spengler, Department of Gastroenterology and Hepatology, University of Wisconsin Hospital and Clinics, Madison, WI 53792, United States

Author contributions: All authors contributed to conception or designing of the work, data collection, drafting manuscript, critical revision of manuscript, final edits and approval the manuscript.

Institutional review board statement: Data was publicly available so IRB approval was not needed.

Conflict-of-interest statement: None of the authors have any conflict of interest.

Data sharing statement: Data was taken by already available public pathologic samples.

CONSORT 2010 statement: The authors have read the CONSORT 2010 statement, and the manuscript was prepared and revised according to the CONSORT 2010 statement.

Corresponding author: Jihad Aljabban, MD, MSc, Academic Research, Doctor, Department of Medicine, University of Wisconsin Hospital and Clinics, 600 Highland Avenue, Madison, WI 53792, United States. jaljabban@uwhealth.org

Received: March 2, 2022
Peer-review started: March 2, 2022
First decision: April 13, 2022
Revised: April 29, 2022
Accepted: June 14, 2022
Article in press: June 14, 2022
Published online: July 27, 2022
Processing time: 147 Days and 12.8 Hours

ARTICLE HIGHLIGHTS

Research background

Non-alcoholic fatty liver disease (NAFLD) pathogenesis is poorly understood but may result from a mix of exogenous and genetic factors that lead to fatty infiltration and inflammation.

Research motivation

NAFLD is a growing cause for liver transplant with limited therapeutic options.

Research objectives

To define genetic changes that underlie NAFLD and progression to non-alcoholic steatohepatitis (NASH) in pursuit of identifying promising therapeutic targets.

Research methods

We employed our STARGEO platform to conduct meta-analyses of publicly available liver biopsies from NAFLD and NASH patients.

Research results

We identified various genes implicated in inflammation and fatty infiltration, as well as signaling processes that lead to these changes. We also identified riciribine and ZSTK-474 as potential drugs.

Research conclusions

NAFLD and its progression to NASH is likely led by several genetic changes detailed in our manuscript. The genetic changes in our dataset are targeted by ricirbine and ZSTK-474 and warrants further study.

Research perspectives

As NAFLD becomes an increasing clinical burden, a bioinformatics approach is valuable in understanding causes and elucidating treatment avenues.