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Gene Therapy in Oral Tissue Regeneration
Published in Vincenzo Guarino, Marco Antonio Alvarez-Pérez, Current Advances in Oral and Craniofacial Tissue Engineering, 2020
Fernando Suaste, Patricia González-Alva, Alejandro Luis, Osmar Alejandro
Moreover, the use of biomaterials to achieve periodontal regeneration such as polymers serve as the delivery system for growth factors and DNA molecules, indicated by the retard apical migration of epithelial cells from the PDL region and alveolar bone. Diverse studies showed that bioresorbable recombinant human Growth/Differentiation Factor-5 (rhGDF-5) with poly(lactic-co-glycolic acid) (PLA) was applied in an in vivo experiment; bone formation was observed after 6 weeks of treatment in sites receiving rhGDF-5/PLGA exhibiting a significant increase in PDL, cementum and bone regeneration (Kwon et al. 2010).
Drug-Related Sarcopenia
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
Genetic factors contribute highly to variability in muscle strength and provide a strong risk factor for the development of sarcopenia among older adults.4 Studies have shown that genes growth/differentiation factor 8 (GDF8), cyclin-dependent kinase inhibitor 1A (CDKN1A), and myogenic differentiation antigen 1 (MYOD1) are possible candidate genes that affect lower extremity muscle strength.4 In regards to the myostatin pathway, cyclin-dependent kinase 2 (CKD2), retinoblastoma (RB1), and IGF01 are correlative to muscle strength.4 Moreover, polymorphisms in the vitamin D receptor (VDR) are also associated with muscle strength, because vitamin D has an effect on both smooth and striated muscle. Genetic research is anticipated to facilitate sarcopenia diagnosis and guide therapies.
Precision medicine in myelodysplastic syndromes
Published in Debmalya Barh, Precision Medicine in Cancers and Non-Communicable Diseases, 2018
Advances in supportive care are connected with advances in MDS molecular biology and pathogenesis research (Gill et al., 2016). A new target has emerged in treating MDS-related anemia. Defects in erythroid differentiation lead to increased production of erythropoietin without effective hemoglobin synthesis. Growth differentiation factor GDF11, an important erythropoiesis regulator, accumulates and can be inhibited by transforming growth factor β (TGF-β) superfamily ligand trap strategies (Dussiot et al., 2014; Suragani et al., 2014). Luspatercept is an activin receptor antagonist that functions as a ligand trap for GDF11 and other TGF-β family ligands to suppress Smad2/3 activation and to increase hemoglobin synthesis (Mies et al., 2016; Almeida et al., 2017).
A population pharmacokinetic-pharmacodynamic model of navtemadlin, its glucuronide metabolite (M1) and serum macrophage inhibitory cykokine-1 (MIC-1)
Published in Xenobiotica, 2022
Lu Zhang, Bill Poland, Michelle Green, Shekman Wong, J. Greg Slatter
Macrophage inhibitory cytokine-1 (MIC-1 or Growth Differentiation Factor 15 [GDF15]), a pleiotropic member of the transforming growth factor-beta family, is expressed in response to various cellular stressors and modifies pro-growth and pro-apoptosis signal transduction pathways, both in cancer cells and in the tumour microenvironment (Tan et al. 2000; Wischhusen et al. 2020). MIC-1 is a direct target of p53 transcriptional activation, and navtemadlin elicits dose-dependent increases of serum MIC-1, with the magnitude of MIC-1 fold change limited by higher baseline MIC-1 concentrations (Allard et al. 2020). Therefore, increases in MIC-1 relative to baseline serum concentrations provide a viable pharmacodynamic (PD) marker of response to MDM2 inhibition by navtemadlin in cancer patients.
Elevated circulating growth differentiation factor 15 is related to decreased heart rate variability in chronic kidney disease patients
Published in Renal Failure, 2021
Lulu Wang, Jing Luo, Wenjin Liu, Xiaoqin Huang, Jie Xu, Yang Zhou, Lei Jiang, Junwei Yang
Growth differentiation factor 15 (GDF15) is a protein of the transforming growth factor beta (TGFβ) superfamily. It was first separated from a U937 subtraction cDNA library and originally named macrophage inhibitory factor 1 (MIC-1) [3]. It was subsequently given the official designation of growth differentiation factor 15 (GDF15) [4] and is also known as prostate differentiation factor, placental TGF-beta, and nonsteroidal anti-inflammatory drug-activated protein-1 [5]. Human GDF15 is localized on chromosome 19 and consists of two exons separated by an intron. GDF15 is first synthesized as an inactive precursor protein with 308 amino acids with a 29-amino-acid signal peptide at the N-terminal region. It is then separated by furin at an RXXR site to yield a propeptide and a mature peptide; the latter is secreted as a dimeric protein of 224 amino acids with a molecular weight of approximately 25 KDa [6,7] and is regarded as the active form of GDF15. GDF15 can specifically bind to GDNF family receptor α-like (GFRAL) with high affinity and forms a complex with RET, the transmembrane tyrosine kinase coreceptor, which subsequently activates intracellular signaling pathways, thereby facilitating several biological effects [8,9]. Previous studies have suggested a link between GDF15 and CVD. A study by Wollert found higher plasma GDF15 levels in patients with cardiovascular events, and the effect was an independent cardiovascular risk factor [10]. However, animal experiments led to diverse conclusions that the protein could inhibit the development of atherosclerosis [11].
Recent Advances in Biomaterials for the Treatment of Bone Defects
Published in Organogenesis, 2020
Le-Yi Zhang, Qing Bi, Chen Zhao, Jin-Yang Chen, Mao-Hua Cai, Xiao-Yi Chen
PDGF promotes the recruitment and proliferation of cells, including MSCs, as well as blood vessel formation at the healing site. In synergistic combination with PLLA/Col/HA and PLLA/HA, PDGF-BB displayed enhanced osteogenic differentiation potential for bone regeneration.88 rhPDGF-BB (Augment bone graft®) was approved in 2015 for hindfoot and ankle fusion in arthritis patients.89 Growth differentiation factor 5 (GDF5) stimulates bone, cartilage, tendon and ligament formation.90 Several preclinical investigations demonstrated the application of rhGDF5 for bone induction and soft tissue growth. BB-1 (GDF-5V453/V456), a mutant growth factor, was developed for bone reconstruction due to its superior BMP receptor-IA binding.91 While both GDF5 and BB-1 displayed high angiogenic potential, BB-1 had greater bone repair capacity.92 TGF-β1 participates in bone remodeling with insulin-like growth factor 1 (IGF-1).3 TGF-β1 regulates osteoclastogenesis and recruits BMMSCs to the repair site, while IGF-1 induces the BMMSC differentiation into osteoblasts. It has been demonstrated that a combination of BMMSCs and IGF-1/TGF-β1 in a laminin gel scaffold improves ameliorates osteochondral defect model.93