Der diesjährige Egon-Nettersheim-Forschungspreis wurde am 26. November 2024 vergeben an Dr. rer. nat. Thuong Trinh-Minh

Name: Thuong Trinh-Minh

DOB: 22.07.1991, in Vietnam

Nationality: Vietnamese

Education and Experience:

• Until now: Scientific Staff & Subgroup Leader, Universitätsklinikum Düsseldorf, Hiller Research Center, Department of Rheumatology, Düsseldorf, Germany

• 2023: Achieve Dr. rer. nat title in Biology from Friedrich-Alexander-University Erlangen-Nürnberg

• 2016–2022: PhD Student, Rheumatology & Immunology, Friedrich-Alexander-University Erlangen-Nürnberg, Germany

• 2015–2016: Project manager and supervisor, Molecular Biology Lab, University of Science, Vietnam

• 2009–2015: Bachelor and Master of Biotechnology, University of Science, Vietnam

Research Summary:

Study Focus: The study investigates the critical role of WNT5A in the pathogenesis of fibrosis, unveiling how WNT5A, through a noncanonical signaling pathway, triggers the activation of latent TGF-beta.

Highlight Points:

• Central Role of TGF-β Signaling: TGF-β signaling is central to fibrosis, but its activation mechanisms were not fully understood.

• WNT5A Identification: WNT5A is identified as a major noncanonical WNT ligand in fibrotic conditions, including systemic sclerosis, chronic graft-versus-host disease, and idiopathic pulmonary fibrosis.

• Mechanism of Activation: WNT5A/JNK/ROCK signaling is crucial for activating latent TGF-β in fibrotic diseases. This process involves:

• Rapid JNK- and ROCK-dependent cytoskeletal rearrangements.

• Generation of contraction-induced forces.

• Activation of TGF-beta through focal adhesions and integrin alpha V (ITGAV).

• Therapeutic Potential: Removing WNT5A or its targets prevented latent TGF-β activation, rebalanced TGF-β signaling, and improved experimental fibrosis. This suggests that targeting WNT5A/JNK/ROCK signaling is a promising new treatment for fibrotic diseases.