Department of Orthopedic Surgery, Mayo Clinic, 200 First Street SW, Rochester, Minnesota.
J Orthop Res. 2019 Jul;37(7):1465-1474. doi: 10.1002/jor.24305. Epub 2019 Apr 25.
Skeletal regenerative medicine aims to repair or regenerate skeletal tissues using pharmacotherapies, cell-based treatments, and/or surgical interventions. The field is guided by biological principles active during development, wound healing, aging, and carcinogenesis. Skeletal development and tissue maintenance in adults represent highly intricate biological processes that require continuous adjustments in the expression of cell type-specific genes that generate, remodel, and repair the skeletal extracellular matrix. Errors in these processes can facilitate musculoskeletal disease including cancers or injury. The fundamental molecular mechanisms by which cell type-specific patterns in gene expression are established and retained during successive mitotic divisions require epigenetic control, which we review here. We focus on epigenetic regulatory proteins that control the mammalian epigenome at the level of chromatin with emphasis on proteins that are amenable to drug intervention to mitigate skeletal tissue degeneration (e.g., osteoarthritis and osteoporosis). We highlight recent findings on a number of druggable epigenetic regulators, including DNA methyltransferases (e.g., DNMT1, DNMT3A, and DNMT3B) and hydroxylases (e.g., TET1, TET2, and TET3), histone methyltransferases (e.g., EZH1, EZH2, and DOT1L) as well as histone deacetylases (e.g., HDAC3, HDAC4, and HDAC7) and histone acetyl readers (e.g., BRD4) in relation to the development of bone or cartilage regenerative drug therapies. We also review how histone mutations lead to epigenomic catastrophe and cause musculoskeletal tumors. The combined body of molecular and genetic studies focusing on epigenetic regulators indicates that these proteins are critical for normal skeletogenesis and viable candidate drug targets for short-term local pharmacological strategies to mitigate musculoskeletal tissue degeneration. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 37:1465-1474, 2019.
骨骼再生医学旨在通过药物治疗、基于细胞的治疗和/或手术干预来修复或再生骨骼组织。该领域的指导原则是在发育、创伤愈合、衰老和癌变过程中发挥作用的生物学原理。成年人的骨骼发育和组织维持代表了高度复杂的生物学过程,需要不断调整生成、重塑和修复骨骼细胞外基质的细胞类型特异性基因的表达。这些过程中的错误会促进包括癌症或损伤在内的肌肉骨骼疾病的发生。在这里,我们回顾了细胞类型特异性基因表达模式在连续有丝分裂分裂过程中建立和保留的基本分子机制。我们专注于控制哺乳动物表观基因组在染色质水平的表观遗传调节蛋白,重点是那些可以通过药物干预来减轻骨骼组织退化(例如,骨关节炎和骨质疏松症)的蛋白。我们强调了一些可药物干预的表观遗传调节剂的最新发现,包括 DNA 甲基转移酶(例如,DNMT1、DNMT3A 和 DNMT3B)和羟化酶(例如,TET1、TET2 和 TET3)、组蛋白甲基转移酶(例如,EZH1、EZH2 和 DOT1L)以及组蛋白去乙酰化酶(例如,HDAC3、HDAC4 和 HDAC7)和组蛋白乙酰基阅读器(例如,BRD4),与骨或软骨再生药物疗法的发展有关。我们还回顾了组蛋白突变如何导致表观基因组灾难并导致肌肉骨骼肿瘤。这些集中在表观遗传调节剂上的分子和遗传研究的综合结果表明,这些蛋白质对于正常的骨骼发生是至关重要的,并且是短期局部药物策略缓解肌肉骨骼组织退化的可行候选药物靶点。©2019 矫形研究学会。由 Wiley 期刊出版公司出版。J Orthop Res 37:1465-1474, 2019.