Fibroblast growth factors: key players in regeneration and tissue repair

Maddaluno, Luigi; Urwyler, Corinne; Werner, Sabine

doi:10.1242/dev.152587

Cited by 198 publications

(159 citation statements)

References 125 publications

(184 reference statements)

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“…An important step in the development of endochondral bone is reactivation based on the time of the bony injury, as most of FGFs and FGFRs seem upregulated during this step. Therefore, this confirms their roles in bone healing (Maddaluno, Urwyler, & Werner, 2017). A recent study has shown that the healing of calvarium defects is directly linked with FGFs.…”

Section: Fibroblast Growth Factorssupporting

confidence: 81%

Bioengineering strategies for bone and cartilage tissue regeneration using growth factors and stem cells

Qasim

Chae

Lee

2019

J Biomedical Materials Res

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Bone and cartilage tissue engineering is an integrative approach that is inspired by the phenomena associated with wound healing. In this respect, growth factors have emerged as important moieties for the control and regulation of this process. Growth factors act as mediators and control the important physiological functions of bone regeneration. Herein, we discuss the importance of growth factors in bone and cartilage tissue engineering, their loading and delivery strategies, release kinetics, and their integration with biomaterials and stem cells to heal bone fractures. We also highlighted the role of growth factors in the determination of the bone tissue microenvironment based on the reciprocal signaling with cells and biomaterial scaffolds on which future bone and cartilage tissue engineering technologies and medical devices will be based upon. K E Y W O R D S biomaterials, bone and cartilage regeneration, growth factor, stem cell, tissue engineering

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Section: Fibroblast Growth Factorssupporting

confidence: 81%

Bioengineering strategies for bone and cartilage tissue regeneration using growth factors and stem cells

Qasim

Chae

Lee

2019

J Biomedical Materials Res

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“…FGF15/19 is secreted from the enterocytes under physiological conditions, circulates to the liver, and activates Fgfr4 in the presence of β‐Klotho. Activation of Fgfr4 leads to activation of several signaling pathways, including MAPK and Stat3, which are believed to be the major mechanism to suppress BA synthesis and promote cell cycle progression . Activation of these pathways could contribute to the priming of liver regeneration.…”

Section: Discussionmentioning

confidence: 99%

“…Activation of Fgfr4 leads to activation of several signaling pathways, including MAPK and Stat3, which are believed to be the major mechanism to suppress BA synthesis and promote cell cycle progression. (13,22,34) Activation of these pathways could contribute to the priming of liver regeneration. The early stage of liver regeneration (approximately 0 hours to 4 hours after PHx in mice) is known as the "priming" phase, which requires an orchestration of various molecular signaling pathways and complex tissue interactions.…”

Section: Discussionmentioning

confidence: 99%

Fibroblast Growth Factor 15–Dependent and Bile Acid–Independent Promotion of Liver Regeneration in Mice

et al. 2018

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The role of intestine-derived factors in promoting liver regeneration after partial hepatectomy (PHx) are not entirely known, but bile acids (BAs) and fibroblast growth factor 15 (Fgf15) that is highly expressed in the mouse ileum could promote hepatocyte proliferation. Fgf15 strongly suppresses the synthesis of BAs, and emerging evidence indicates that Fgf15 is important for liver regeneration. The mechanisms by which Fgf15 promotes liver regeneration are unclear, but Fgf15 may do so indirectly by reducing BA levels and/or directly by promoting cell proliferation. However, it remains undetermined whether these two mechanisms are independent or integrated. In this study, we aimed to clarify these relationships by generating Fgf15 Tet-Off, transgenic mice (Fgf15 Tg) that had very low BA levels as a result from overexpressed Fgf15-mediated suppression of BA synthesis. Compared with wild-type mice, the Fgf15 Tg mice showed increased hepatocyte proliferation even without surgery, and a further induction of the genes in cell-cycle progression after PHx. Moreover, overexpression of Fgf15 by adeno-associated virus (AAV)-Fgf15 transduction or treatment with the recombinant Fgf15 protein led to increased cell proliferation in vivo. Furthermore, Fgf15 Tg mice exhibited an earlier and greater activation of mitogen-activated protein kinase, signal transducer and activator of transcription 3, and NF-κB signaling pathways in the priming stage, and a disruption of the hippo signaling pathway in the termination stage of liver regeneration. Conclusion: Direct in vivo evidence demonstrates that Fgf15 is critical in stimulating the phases of priming and termination of liver regeneration that are critical for cell survival and liver-size determination, independent of BA levels. (Hepatology 2018; 00:000-000).

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“…Growth factors in the inflammatory phase initiate angiogenesis and granulation by excreting growth factors such as TGF-β, IGF-1, MIP-1, MCP-2, TNF-α that trigger cell movement into the wound and play an important role in extracellular matrix formation. Growth factors VEGF and iNOS promote angiogenic activity [32]. The inflammatory phase follows the phase of proliferation characterized by tissue granulation and angiogenesis.…”

Section: Role Of Dpp Iv/cd26 In Wound Healing In Diabetesmentioning

confidence: 99%

Wound Healing Process, Diabetes and Implications of Dipeptidyl Peptidase IV (DPP IV/CD26)

Pučar¹,

Kovač²,

Detel³

et al. 2017

J Tissue Sci Eng

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Dipeptidyl Peptidase IV or molecule CD26 (DPP IV/CD26) is a multifunctional protein, identified as a therapeutic target for type 2 diabetes, due to its ability to degrade incretins, insulin secretagogues. Delayed wound healing is a significant complication in diabetic patients that represents a major socio-economic health problem. It has been proposed that DPP IV/CD26 inhibition accelerates healing of chronic diabetic ulcers in those patients, through the induction of a histological pattern consistent with enhanced angiogenesis. Studies on mice models of diabetesdisturbed wound healing also suggested that the inhibition of DPP IV enzymatic activity may improve tissue regeneration processes. However, further research is needed to elucidate the role of DPP IV/CD26 in diabetic wound healing. The objective of this work was to discuss recent findings on the implications of DPP IV/CD26 in tissue regeneration and reparation in diabetic environment.

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Fibroblast growth factors: key players in regeneration and tissue repair

Cited by 198 publications

References 125 publications

Bioengineering strategies for bone and cartilage tissue regeneration using growth factors and stem cells

Bioengineering strategies for bone and cartilage tissue regeneration using growth factors and stem cells

Fibroblast Growth Factor 15–Dependent and Bile Acid–Independent Promotion of Liver Regeneration in Mice

Wound Healing Process, Diabetes and Implications of Dipeptidyl Peptidase IV (DPP IV/CD26)

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