Oral Biomedicine ›› 2021, Vol. 12 ›› Issue (1): 1-4.
1,Zhuan Bian
Received:2021-02-22
Revised:2021-03-05
Online:2021-03-25
Published:2021-04-01
Contact:
Zhuan Bian
E-mail:bianzhuan@whu.edu.cn
Zhuan Bian. Research progress on the etiology and pathogenic mechanism of hereditary gingival fibromatosis[J]. Oral Biomedicine, 2021, 12(1): 1-4.
Add to citation manager EndNote|Reference Manager|ProCite|BibTeX|RefWorks
| [1] | Ye X, Shi L, Cheng Y, et al.A novel locus for autosomal dominant hereditary gingival fibromatosis,GINGF3,maps to chromosome 2p223-p23.3[J].Clin Genet, 2005, 68(3):239-244 |
| [2] | Ye X, Shi L, Yin W, et al.Further evidence of genetic heterogeneity segregating with hereditary gingival fibromatosis[J].J Clin Periodontol, 2009, 36(8):627-633 |
| [3] | Hart TC, Zhang Y, Gorry MC, et al.A mutation in the SOS1 gene causes hereditary gingival fibromatosis type 1[J].Am J Hum Genet, 2002, 70(4):943-954 |
| [4] | Jang SI, Lee EJ, Hart PS, et al.Germ line gain of function with SOS1 mutation in hereditary gingival fibromatosis[J].J Biol Chem, 2007, 282(28):20245-20255 |
| [5] | Bayram Y, White JJ, Elcioglu N, et al.REST final-exon-truncating mutations cause hereditary gingival fibromatosis[J].Am J Hum Genet, 2017, 101(1):149-156 |
| [6] | Nishimura F, Naruishi H, Naruishi K, et al.Cathepsin-L, a key molecule in the pathogenesis of drug-induced and I-cell disease-mediated gingival overgrowth: a study with cathepsin-L-deficient mice[J].Am J Pathol, 2002, 161(6):2047-2052 |
| [7] | Kortüm F, Caputo V, Bauer CK, et al.Mutations in KCNH1 and ATP6V1B2 cause Zimmermann-Laband syndrome[J].Nat Genet, 2015, 47(6):661-667 |
| [8] | Tommiska J, K?ns?koski J, Skibsbye L, et al.Two missense mutations in KCNQ1 cause pituitary hormone deficiency and maternally inherited gingival fibromatosis[J].Nat Commun, 2017, 8(1):1289- |
| [9] | Brownstein CA, Towne MC, Luquette LJ, et al.Mutation of KCNJ8 in a patient with Cantú syndrome with unique vascular abnormalities - support for the role of K(ATP) channels in this condition[J].Eur J Med Genet, 2013, 56(12):678-682 |
| [10] | Cooper PE, Reutter H, Woelfle J, et al.Cantú syndrome resulting from activating mutation in the KCNJ8 gene[J].Hum Mutat, 2014, 35(7):809-813 |
| [11] | van Bon BW, Gilissen C, Grange DK, et al.Cantú syndrome is caused by mutations in ABCC9[J].Am J Hum Genet, 2012, 90(6):1094-1101 |
| [12] | Pachajoa H, López-Quintero W, Vanegas S, et al.Novel mutation in ABBC9 gene associated with congenital hypertrichosis and acromegaloid facial features,without cardiac or skeletal anomalies: A new phenotype[J].Appl Clin Genet, 2018, 11:15-21 |
| [13] | Brohawn SG, Campbell EB, MacKinnon R.Physical mechanism for gating and mechanosensitivity of the human TRAAK K^+ channel[J].Nature, 2014, 516(7529):126-130 |
| [14] | Bauer CK, Calligari P, Radio FC, et al.Mutations in KCNK4 that affect gating cause a recognizable neurodevelopmental syndrome[J].Am J Hum Genet, 2018, 103(4):621-630 |
| [15] | Mariani P, Zhurakivska K, Santoro R, et al.Hereditary gingival fibromatosis associated with the missense mutation of the KCNK4 gene[J].Oral Surg Oral Med Oral Pathol Oral Radiol, 2020, :S2212-4403(20)31128-7- |
| [16] | Gao Q, Yang CC, Meng LY, et al.Activated KCNQ1 channel promotes fibrogenic response in hereditary gingival fibromatosis via clustering and activation of Ras[J].J Periodontal Res, 2020, :- |
| [17] | Zhou Y, Wong CO, Cho KJ, et al.SIGNAL TRANSDUCTION. Membrane potential modulates plasma membrane phospholipid dynamics and K-Ras signaling[J].Science, 2015, 349(6250):873-876 |
| [18] | Gao Q, Yang K, Chen D, et al.Antifibrotic potential of MiR-335-3p in hereditary gingival fibromatosis[J].J Dent Res, 2019, 98(10):1140-1149 |
| [19] | H?kkinen L, Csiszar A.Hereditary gingival fibromatosis: Characteristics and novel putative pathogenic mechanisms[J].J Dent Res, 2007, 86(1):25-34 |
| [20] | Evans BR, Mosig RA, Lobl M, et al.Mutation of membrane type-1 metalloproteinase, MT1-MMP, causes the multicentric osteolysis and arthritis disease Winchester syndrome[J].Am J Hum Genet, 2012, 91(3):572-576 |
| [21] | Grover S, Grewal RS, Verma R, et al.Winchester syndrome: A case report[J].Int J Dermatol, 2009, 48(2):175-177 |
| [22] | Bhavani GS, Shah H, Shukla A, et al.Clinical and mutation profile of multicentric osteolysis nodulosis and arthropathy[J].Am J Med Genet A, 2016, 170A(2):410-417 |
| [23] | Van Damme T, Colige A, Syx D, et al.Expanding the clinical and mutational spectrum of the Ehlers-Danlos syndrome,dermatosparaxis type[J].Genet Med, 2016, 18(9):882-891 |
| [24] | Hanks S, Adams S, Douglas J, et al.Mutations in the gene encoding capillary morphogenesis protein 2 cause juvenile hyaline fibromatosis and infantile systemic hyalinosis[J].Am J Hum Genet, 2003, 73(4):791-800 |
| [25] | Wang YY, Wen CQ, Wei Z, et al.A novel splice site mutation in ANTXR2 (CMG2) gene results in systemic hyalinosis[J].J Pediatr Hematol Oncol, 2011, 33(8):e355-e357 |
| [26] | Denadai R, Raposo-Amaral CE, Bertola D, et al.Identification of 2 novel ANTXR2 mutations in patients with hyaline fibromatosis syndrome and proposal of a modified grading system[J].Am J Med Genet A, 2012, 158A(4):732-742 |
| [27] | Wilson GR, Sunley J, Smith KR, et al.Mutations in SH3PXD2B cause Borrone dermato-cardio-skeletal syndrome[J].Eur J Hum Genet, 2014, 22(6):741-747 |
| [28] | Parker K, Pabla R, Hay N, et al.Common dental features and craniofacial development of three siblings with Ter Haar syndrome[J].Eur Arch Paediatr Dent, 2014, 15(1):59-64 |
| [29] | Tefs K, Gueorguieva M, Klammt J, et al.Molecular and clinical spectrum of type I plasminogen deficiency: A series of 50 patients[J].Blood, 2006, 108(9):3021-3026 |
| [30] | Itoh Y.Membrane-type matrix metalloproteinases: Their functions and regulations[J].Matrix Biol, 2015, 444546:207-223 |
| [31] | Reeves C, Charles-Horvath P, Kitajewski J.Studies in mice reveal a role for Anthrax toxin receptors in matrix metalloproteinase function and extracellular matrix homeostasis[J].Toxins (Basel), 2013, 5(2):315-326 |
| [32] | Deryugina EI, Quigley JP.Cell surface remodeling by plasmin: A new function for an old enzyme[J].J Biomed Biotechnol, 2012, 2012:564259- |
| [33] | Buschman MD, Bromann PA, Cejudo-Martin P, et al.The novel adaptor protein Tks4 (SH3PXD2B) is required for functional podosome formation[J].Mol Biol Cell, 2009, 20(5):1302-1311 |
| [34] | Iizuka S, Abdullah C, Buschman MD, et al.The role of Tks adaptor proteins in invadopodia formation, growth and metastasis of melanoma[J].Oncotarget, 2016, 7(48):78473-78486 |
| [35] | Bekhouche M, Leduc C, Dupont L, et al.Determination of the substrate repertoire of ADAMTS2, 3, and 14 significantly broadens their functions and identifies extracellular matrix organization and TGF-β signaling as primary targets[J].FASEB J, 2016, 30(5):1741-1756 |
| [36] | Coletta RD, Graner E.Hereditary gingival fibromatosis: A systematic review[J].J Periodontol, 2006, 77(5):753-764 |
| [37] | Meng LY, Huang MJ, Ye XQ, et al.Increased expression of collagen prolyl 4-hydroxylases in Chinese patients with hereditary gingival fibromatosis[J].Arch Oral Biol, 2007, 52(12):1209-1214 |
| [38] | Roman-Malo L, Bullon B, de Miguel M, et al.Fibroblasts collagen production and histological alterations in hereditary gingival fibromatosis[J].Diseases, 2019, 7(2):39- |
| [39] | Gawron K, ?azarz-Bartyzel K, Kowalska A, et al.Fibroblasts from recurrent fibrotic overgrowths reveal high rate of proliferation in vitro-findings from the study of hereditary and idiopathic gingival fibromatosis[J].Connect Tissue Res, 2019, 60(1):29-39 |
| [40] | Meng LY, Ye XQ, Fan MW, et al.Keratinocytes modify fibroblast metabolism in hereditary gingival fibromatosis[J].Arch Oral Biol, 2008, 53(11):1050-1057 |
| [41] | Hazzaa HH, Gouda OM, Kamal NM, et al.Expression of CD163 in hereditary gingival fibromatosis: A possible association with TGF-β1[J].J Oral Pathol Med, 2018, 47(3):286-292 |
| [42] | Nowarski R, Jackson R, Flavell RA.The stromal intervention: Regulation of immunity and inflammation at the epithelial-mesenchymal barrier[J].Cell, 2017, 168(3):362-375 |
| [43] | Wu CF, Chiang WC, Lai CF, et al.Transforming growth factor β-1 stimulates profibrotic epithelial signaling to activate pericyte-myofibroblast transition in obstructive kidney fibrosis[J].Am J Pathol, 2013, 182(1):118-131 |
| No related articles found! |
| Viewed | ||||||
|
Full text |
|
|||||
|
Abstract |
|
|||||
