Tom Lüdde

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Academic Career Length

24Years (2003-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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3 June 2019 in Nature Medicine

Journal Article

Deep learning can predict microsatellite instability directly from histology in gastrointestinal cancer

Alexander T. Pearson

Dirk Jäger

+11

4 February 2011 in Nature Reviews Gastroenterology & Hepatology

Journal Article

NF-κB in the liver—linking injury, fibrosis and hepatocellular carcinoma

Tom Lüdde

Robert F. Schwabe

20 August 2010 in Hepatology

Journal Article

Micro-RNA profiling reveals a role for miR-29 in human and murine liver fibrosis

Christoph Roderburg

Gerd-Willem Urban

Kira Bettermann

Mihael Vucur

Henning Zimmermann

Tom Lüdde

Liver fibrosis is orchestrated by a complex network of signaling pathways regulating the deposition of extracellular matrix proteins during fibrogenesis. MicroRNAs (miRNAs) represent a family of small noncoding RNAs controlling translation and transcription of many genes. Recently, miRNAs have been suggested to crucially modulate cellular processes in the liver such as hepatocarcinogenesis. However, their role in liver fibrosis is not well understood. We systematically analyzed the regulation of miRNAs in a mouse model of carbon tetrachloride–induced hepatic fibrogenesis (CCl4) by gene array analysis, which revealed a panel of miRNA that were specifically regulated in livers of mice undergoing hepatic fibrosis. Within those, all three members of the miR-29-family were significantly down-regulated in livers of CCl4-treated mice as well as in mice that underwent bile duct ligation. Specific regulation of miR-29 members in murine fibrosis models correlated with lower expression of miR-29 in livers from patients with advanced liver fibrosis. Moreover, patients with advanced liver cirrhosis showed significantly lower levels of miR-29a in their serum when compared with healthy controls or patients with early fibrosis. On a cellular level, down-regulation of miR-29 in murine hepatic stellate cells (HSCs) was mediated by transforming growth factor beta (TGF-β) as well as inflammatory signals, namely, lipopolysaccharide (LPS) and nuclear factor kappa B (NF-κB). Furthermore, overexpression of miR-29b in murine HSC resulted in down-regulation of collagen expression. Conclusion: Our data indicate that miR-29 mediates the regulation of liver fibrosis and is part of a signaling nexus involving TGF-β- and NF-κB–dependent down-regulation of miR-29 family members in HSC with subsequent up-regulation of extracellular matrix genes. Thus they may represent targets for novel therapeutic strategies against hepatic fibrogenesis and also might evolve as biomarkers in the diagnosis of liver fibrosis. (Hepatology 2011.)