PDF(Pubmed)
Abstract：
The formation of bone outside the normal skeleton, or heterotopic ossification (HO), occurs through genetic and acquired mechanisms. Fibrodysplasia ossificans progressiva (FOP), the most devastating genetic condition of HO, is due to mutations in the ACVR1/ALK2 gene and is relentlessly progressive. Acquired HO is mostly precipitated by injury or orthopedic surgical procedures but can also be associated with certain conditions related to aging. Cellular senescence is a hallmark of aging and thought to be a tumor-suppressive mechanism with characteristic features such as irreversible growth arrest, apoptosis resistance, and an inflammatory senescence-associated secretory phenotype (SASP). Here, we review possible roles for cellular senescence in HO and how targeting senescent cells may provide new therapeutic approaches to both FOP and acquired forms of HO.
摘要：
正常骨骼外骨的形成，或异位骨化(HO)，通过遗传和后天机制发生。进行性骨化性纤维发育不良（FOP），HO最具破坏性的遗传条件，是由于ACVR1/ALK2基因的突变，并且是无情地进行性的。获得的HO主要是由损伤或整形外科手术引起的，但也可能与某些与衰老相关的疾病有关。细胞衰老是衰老的标志，被认为是一种肿瘤抑制机制，具有不可逆的生长停滞等特征。凋亡抗性，和炎性衰老相关分泌表型（SASP）。这里,我们回顾了细胞衰老在HO中的可能作用，以及靶向衰老细胞如何为FOP和获得性HO提供新的治疗方法。
