Bradley Elizabeth W, Carpio Lomeli R, van Wijnen Andre J, McGee-Lawrence Meghan E, Westendorf Jennifer J
Mayo Clinic, Departments of Orthopedic Surgery and of Biochemistry and Molecular Biology, and Mayo Graduate School, Rochester, Minnesota; and Georgia Regents University, Department of Cellular Biology and Anatomy, Augusta, Georgia.
Physiol Rev. 2015 Oct;95(4):1359-81. doi: 10.1152/physrev.00004.2015.
Histone deacetylases (Hdacs) are conserved enzymes that remove acetyl groups from lysine side chains in histones and other proteins. Eleven of the 18 Hdacs encoded by the human and mouse genomes depend on Zn(2+) for enzymatic activity, while the other 7, the sirtuins (Sirts), require NAD2(+). Collectively, Hdacs and Sirts regulate numerous cellular and mitochondrial processes including gene transcription, DNA repair, protein stability, cytoskeletal dynamics, and signaling pathways to affect both development and aging. Of clinical relevance, Hdacs inhibitors are United States Food and Drug Administration-approved cancer therapeutics and are candidate therapies for other common diseases including arthritis, diabetes, epilepsy, heart disease, HIV infection, neurodegeneration, and numerous aging-related disorders. Hdacs and Sirts influence skeletal development, maintenance of mineral density and bone strength by affecting intramembranous and endochondral ossification, as well as bone resorption. With few exceptions, inhibition of Hdac or Sirt activity though either loss-of-function mutations or prolonged chemical inhibition has negative and/or toxic effects on skeletal development and bone mineral density. Specifically, Hdac/Sirt suppression causes abnormalities in physiological development such as craniofacial dimorphisms, short stature, and bone fragility that are associated with several human syndromes or diseases. In contrast, activation of Sirts may protect the skeleton from aging and immobilization-related bone loss. This knowledge may prolong healthspan and prevent adverse events caused by epigenetic therapies that are entering the clinical realm at an unprecedented rate. In this review, we summarize the general properties of Hdacs/Sirts and the research that has revealed their essential functions in bone forming cells (e.g., osteoblasts and chondrocytes) and bone resorbing osteoclasts. Finally, we offer predictions on future research in this area and the utility of this knowledge for orthopedic applications and bone tissue engineering.
组蛋白去乙酰化酶(Hdacs)是一类保守的酶,可去除组蛋白和其他蛋白质赖氨酸侧链上的乙酰基。人类和小鼠基因组编码的18种Hdacs中有11种的酶活性依赖于Zn(2+),而另外7种,即沉默调节蛋白(Sirts),则需要NAD2(+)。总的来说,Hdacs和Sirts调节众多细胞和线粒体过程,包括基因转录、DNA修复、蛋白质稳定性、细胞骨架动力学和信号通路,从而影响发育和衰老。在临床方面,Hdacs抑制剂是美国食品药品监督管理局批准的癌症治疗药物,也是治疗其他常见疾病的候选疗法,这些疾病包括关节炎、糖尿病、癫痫、心脏病、HIV感染、神经退行性疾病以及许多与衰老相关的疾病。Hdacs和Sirts通过影响膜内成骨和软骨内成骨以及骨吸收,从而影响骨骼发育、矿物质密度维持和骨强度。除了少数例外,通过功能丧失突变或长期化学抑制来抑制Hdac或Sirt活性,会对骨骼发育和骨矿物质密度产生负面和/或毒性影响。具体而言,Hdac/Sirt抑制会导致生理发育异常,如颅面二态性、身材矮小和骨脆性,这些都与几种人类综合征或疾病有关。相比之下,Sirts的激活可能会保护骨骼免受衰老和固定相关的骨质流失影响。这一知识可能会延长健康寿命,并预防由以前所未有的速度进入临床领域的表观遗传疗法引起的不良事件。在这篇综述中,我们总结了Hdacs/Sirts的一般特性以及揭示它们在骨形成细胞(如成骨细胞和软骨细胞)和骨吸收破骨细胞中重要功能的研究。最后,我们对该领域未来的研究以及这些知识在骨科应用和骨组织工程中的实用性进行了预测。