Yu Lin, M. O., Sampath, D., Bosykh, D. A., Wang, C., Wang, X., Subramaniam, T., Han, W., Hong, W., & Chakraborty, S. (2024). YAP/TAZ Drive Agrin–Matrix Metalloproteinase 12–Mediated Diabetic Skin Wound Healing. Journal of Investigative Dermatology. https://doi.org/10.1016/j.jid.2024.05.005
Abstract:
The skin tissue is composed of an outer keratinized epidermis underlined by the extracellular matrix (ECM)-rich dermis. Skin injury elicits a complex cascade of highly coordinated molecular events that orchestrate skin wound healing (Eming et al, 2014; Gurtner et al, 2008; Singer and Clark, 1999). Under normal scenarios, skin wounds are healed rapidly with the immediate formation of a clot, followed by an inflammatory response that is essential for recruiting the immune cells, fibroblasts, and blood vessels that contribute to the formation of granulation tissue. Timely induction of these early events sets the stage for the forward migration of the injured epidermal edges that subsequently cover the denuded wound surface through a process called re-epithelization (Martin, 1997). Besides being the major depositor of ECM, the dermal fibroblasts crosstalk with other skin cell types in the wound bed, representing the active mediators of inflammatory and proliferative phases of wound healing (Stunova and Vistejnova, 2018). Failure to orchestrate this sequential healing response is associated with chronic defects in wound healing, which is a major cause of diabetes-associated mortalities (Armstrong et al, 2017). Remodeling of the ECM is foundational to normal wound healing tissue microenvironment because portions of the ECM are lost during injury. In this regard, timely deposition of key ECM proteins to the injured tissues is essential for the functional collaboration between epidermal and dermal cells in promoting the healing response. As such, the scaffolding and signaling properties of key ECM proteins are of utmost interest toward the development of an efficient wound recovery program, especially for patients with diabetes with chronic foot ulcers (Patel et al, 2019; Schultz and Wysocki, 2009; Yildirimer et al, 2012).
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Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)
Funding Info:
This research / project is supported by the Agency for Science, Technology and Research (A*STAR) - Additive Manufacturing for Biological Materials Grant
Grant Reference no. : A18A8b0059
This research is supported by core funding from: Department of Pharmacology and Therapeutics, Roswell Park Comprehensive Cancer Center
Grant Reference no. : NA
This research is supported by core funding from: Institute of Molecular and Cell Biology
Grant Reference no. : NA
This research / project is supported by the Roswell Park’s Scientific Editing and Research Communications Core Resource - National Cancer Institute Cancer Center Support Grant
Grant Reference no. : NCI P30CA016056