Krieg, Thomas - SRG 02
The role of activated fibroblasts in fibrosis – scleroderma as a model disease
Prof. Dr. Dr. h.c. Thomas Krieg
Translational Matrix Biology
CMMC - PI - SRG 02
Executive Board Member
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Translational Matrix Biology
Joseph-Stelzmann-Str. 52
50931 Cologne
Introduction
Alteration of connective tissue is a hallmark of many common diseases. A tightly controlled balance of synthesis and degradation is crucial for guaranteeing the physiological function of bone, cartilage, tendon and skin and all other organs in which connective tissue represents the scaffold.
Our group concentrates on skin diseases with the aim to unravel the cellular and molecular basis of fibrotic and degenerative processes. These are common burdens leading to chronic ulcerations, inadequate healing, reduced strength or fibrotic responses. The resulting diseases represent a major medical and socio-economic problem, and care for these patients needs to be improved.
Our Aims
The Krieg lab aims to better understand mechanisms controlling activation of fibroblasts with a special focus on activation by fibroblast communication with the surrounding extracellular matrix (ECM).
We want to translate our findings into understanding the molecular basis of diseases associated with excessive fibroblast activation and to design targeted therapies.
Our group aims at investigating the mechanisms underlying the control of connective tissue synthesis and the role of cell-matrix interactions.
Fibroblasts represent a heterogeneous group of cells, which derive from different cellular origins, and are the key cells orchestrating the formation of connective tissues following any type of injury. Their phenotype and function are regulated by interactions with the surrounding extracellular matrix (ECM), mediated by specific receptors, and by the activity of growth factors and cytokines through complex paracrine and autocrine regulatory loops.
As a model we use fibroblasts obtained from patients with scleroderma, an autoimmune-driven chronic fibrotic disease that involves the skin but can also affect many other organs. To ensure that results from our experimental work gain direct entry into translational applications, we have initiated a large clinical network for scleroderma patients together with the Department of Dermatology.
Lab website
For more information, please check the research site.
Publications generated during 1/2023-12/2025 with CMMC affiliation
2024 (up to June)
- Raote I, Rosendahl AH, Hakkinen HM, Vibe C, Kucukaylak I, Sawant M, Keufgens L, Frommelt P, Halwas K, Broadbent K, Cunquero M, Castro G, Villemeur M, Nuchel J, Bornikoel A, Dam B, Zirmire RK, Kiran R, Carolis C, Andilla J, Loza-Alvarez P, Ruprecht V, Jamora C, Campelo F, Kruger M, Hammerschmidt M, Eckes B, Neundorf I, Krieg T, and Malhotra V (2024). TANGO1 inhibitors reduce collagen secretion and limit tissue scarring. Nat Commun15, 3302. doi:10.1038/s41467-024-47004-1.
2023
- Hassan N, Krieg T, Zinser M, Schroder K, and Kroger N (2023). An Overview of Scaffolds and Biomaterials for Skin Expansion and Soft Tissue Regeneration: Insights on Zinc and Magnesium as New Potential Key Elements. Polymers (Basel) 15. doi:10.3390/polym15193854.
- Sawant M, Wang F, Koester J, Niehoff A, Nava MM, Lundgren-Akerlund E, Gullberg D, Leitinger B, Wickstrom S, Eckes B, and Krieg T (2023). Ablation of integrin-mediated cell-collagen communication alleviates fibrosis. Ann Rheum Dis 82, 1474-1486. doi:10.1136/ard-2023-224129.