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多囊卵巢综合征卵巢颗粒细胞凋亡研究进展 被引量:10

Research Progress of Granulosa Cell Apoptosis in Polycystic Ovary Syndrome
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摘要 多囊卵巢综合征(PCOS)是一种以内分泌紊乱为主、多种代谢异常导致的异质性临床综合征。PCOS患者双侧卵巢有大量窦卵泡存在,但是不能周期性产生成熟卵泡,其病理机制尚不清楚。目前认为原发性、内在性卵泡生长异常可能是引起PCOS不排卵及临床内分泌改变的病理基础。研究表明,内在性的卵泡发育异常可能与卵巢颗粒细胞的凋亡调控失常有关。通过对PCOS患者卵巢颗粒细胞凋亡的研究,为PCOS病理机制研究提供相关的理论依据,为临床治疗提供新的方向和途径。 Polycystic ovary syndrome (PCOS) is a heterogeneous clinical syndrome caused by multiple metabolic abnormalities especially endocrine disorders. A large number of antral follicles are presented in both ovaries of PCOS patients, but mature follicles can't be produced periodically, and its pathological mechanisms are unclear. Present studies suggest that the primary, intrinsic abnormalities of follicular growth might be the pathological basis of anovulation and clinical endocrine disturbance in PCOS. Studies have shown thai the intrinsic follicular dysplasia may be associated with the regulation disorders of ovarian granulosa cell apoptosis. Researches on ovarian granulosa cell apoptosis in PCOS patients will provide related theoretical evidences for the investigation of its pathological mechanisms as well as bring new directions and means for clinical treatments.
出处 《国际生殖健康/计划生育杂志》 CAS 2009年第5期331-333,340,共4页 Journal of International Reproductive Health/Family Planning
关键词 颗粒细胞 凋亡 多囊卵巢综合征 卵泡 Granulosa cell Apoptosis Polycystic ovarian syndrome Follicle
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  • 1Matsuda-Minehata F, Inoue N, Goto Y, et al. Regulation of ovarian granulosa cell death by pro- and anti-apopotic molecules[J]. J Reprod Dev, 2006, 52(6): 695-705.
  • 2Hussein MR. Apoptosis in the ovary : molecular mechanisms [J]. Hum Reprod Update, 2005, 11 ( 2 ) : 161-177.
  • 3Inoue N, Maeda A, Matsuda-Minehata F, et al. Expression and localization of Fas ligand and Fas during atresia in porcine ovarian follicles[J]. J Reprod Dev, 2006, 52(6): 723-730.
  • 4Vital-Reyes V, Rodriguez-Burford C, Chhieng DC, et al.Ovarian expression of markers associated with proliferation or apoptosis in women with diminished ovarian reserve[J]. Fertil Steril, 2006, 86(1): 176-185.
  • 5Buchsbaum DJ, Zhou T, Lobuglio AF, et al. TRAIL receptor-targeted therapy[J]. Future Oncol, 2006, 2(4): 493-508.
  • 6Jaskelainen M, Kyranlahti A, Anttonen M, et al. TRAIL pathway components and their putative role in granulosa cell apoptosis in the human ovary[J]. Differentiation, 2009, 77(4): 369-376.
  • 7Das M, Djahanbakheh O, Hacihanefioglu B, et al. Granulosa cell survival and proliferation are altered in polycystic ovary syndrome[J]. J Clin Endocrinal Metab, 2008, 93(3):881-887.
  • 8Stubbs SA, Stark J, Dilworth SM, et al. Abnormal preantral folliculogenesis in polycystic ovaries is associated with increased granulosa cell division [J]. J Clin Endocrinol Metab, 2007, 92(11): 4418-4426.
  • 9Honnma H, Endo T, Henmi H, et al. Altered expression of Fas/Fas ligand/caspase8 and membrane type1-matrix metalloproteinase in atretic follicles within dehydroepiandrosterone-induced polycystic ovaries in rats[J]. Apoptosis, 2006, 11(9): 1525-1533.
  • 10Schimmer AD, Dalili S, Batey RA, et al. Targeting XIAP for treatment of malignancy[J]. Cell Death Differ, 2006, 13(2): 179-188.

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