Fibromodulin (FMOD) is known as one of very important extracellular matrix small leucine-rich proteoglycans. This small leucine-rich proteoglycan has critical roles in the extracellular matrix organization and necessary for repairing of tissue in many organs. Given that the major task of FMOD is the modulation of collagen fibrillogenesis. However, recently observed that FMOD plays very important roles in the modulation of a variety of pivotal biological processes including angiogenesis, regulation of TGF-β activity, and differentiation of human fibroblasts into pluripotent cells, inflammatory mechanisms, apoptosis and metastatic related phenotypes. Besides these roles, FMOD has been considered as a new tumor-related antigen in some malignancies such as lymphoma, leukemia, and leiomyoma. Taken together, these findings proposed that FMOD could be introduced as diagnostic and therapeutic biomarkers in treatment of various cancers. Herein, for first time, we highlighted the various roles of FMOD in the cancerous conditions. Moreover, we summarized the diagnostic and therapeutic applications of FMOD in cancer therapy.
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http://dx.doi.org/10.1186/s12935-019-0870-6 | DOI Listing |
ACS Biomater Sci Eng
January 2025
J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, Florida 32611, United States.
The complexation of nucleic acids and collagen forms a platform biomaterial greater than the sum of its parts. This union of biomacromolecules merges the extracellular matrix functionality of collagen with the designable bioactivity of nucleic acids, enabling advances in regenerative medicine, tissue engineering, gene delivery, and targeted therapy. This review traces the historical foundations and critical applications of DNA-collagen complexes and highlights their capabilities, demonstrating them as biocompatible, bioactive, and tunable platform materials.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Chitkara College of Pharmacy, Chitkara University, Rajpura, 140401, Punjab, India.
A diabetic wound (DW) is an alteration in the highly orchestrated physiological sequence of wound healing especially, the inflammatory phase. These alterations result in the generation of oxidative stress and inflammation at the injury site. This further leads to the impairment in the angiogenesis, extracellular matrix, collagen deposition, and re-epithelialization.
View Article and Find Full Text PDFACS Macro Lett
January 2025
Materials Science and Engineering Department, Technion-Israel Institute of Technology, Haifa 3200003, Israel.
In complex networks and fluids such as the extracellular matrix, the mechanical properties are substantially affected by the movement of polymers both part of and entrapped in the network. As many cells are sensitive to the mechanical remodeling of their surroundings, it is important to appreciate how entrapped polymers may inhibit or facilitate remodeling in the network. Here, we explore a molecular-level understanding of network remodeling in a complex hydrogel environment through successive compressive loading and the role that noninteracting polymers may play in a dynamic network.
View Article and Find Full Text PDFJ Mater Chem B
January 2025
Biomaterials Drug Delivery and Nanotechnology Unit, Centre for Biomedical and Biomaterials Research (CBBR), University of Mauritius, Réduit, Mauritius.
Tissue regeneration after a wound occurs through three main overlapping and interrelated stages namely inflammatory, proliferative, and remodelling phases, respectively. The inflammatory phase is key for successful tissue reconstruction and triggers the proliferative phase. The macrophages in the non-healing wounds remain in the inflammatory loop, but their phenotypes can be changed interactions with nanofibre-based scaffolds mimicking the organisation of the native structural support of healthy tissues.
View Article and Find Full Text PDFCNS Neurosci Ther
January 2025
Children's Medical Center, Department of Pediatric Neurology, Peking University First Hospital, Beijing, China.
Aims: Alexander disease (AxD) is a leukodystrophy caused by mutations in the astrocytic filament gene GFAP. There are currently no effective treatments for AxD. Previous studies have rarely established AxD models with the patient's original GFAP mutations.
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