De Masi Alessia, Zanou Nadège, Strotjohann Keno, Lee Dohyun, Lima Tanes I, Li Xiaoxu, Jeon Jongsu, Place Nicolas, Jung Hoe-Yune, Auwerx Johan
Laboratory of Integrative Systems Physiology, Institute of Bioengineering, École Polytechnique Fédérale de Lausanne, Lausanne, 1015, Switzerland.
Institute of Sport Sciences and Department of Biomedical Sciences, Faculty of Biology-Medicine, University of Lausanne, Lausanne, 1015, Switzerland.
Adv Sci (Weinh). 2024 Jul;11(28):e2305927. doi: 10.1002/advs.202305927. Epub 2024 May 10.
Among the inherited myopathies, a group of muscular disorders characterized by structural and metabolic impairments in skeletal muscle, Duchenne muscular dystrophy (DMD) stands out for its devastating progression. DMD pathogenesis is driven by the progressive degeneration of muscle fibers, resulting in inflammation and fibrosis that ultimately affect the overall muscle biomechanics. At the opposite end of the spectrum of muscle diseases, age-related sarcopenia is a common condition that affects an increasing proportion of the elderly. Although characterized by different pathological mechanisms, DMD and sarcopenia share the development of progressive muscle weakness and tissue inflammation. Here, the therapeutic effects of Cyclo Histidine-Proline (CHP) against DMD and sarcopenia are evaluated. In the mdx mouse model of DMD, it is shown that CHP restored muscle contractility and force production, accompanied by the reduction of fibrosis and inflammation in skeletal muscle. CHP furthermore prevented the development of cardiomyopathy and fibrosis in the diaphragm, the two leading causes of death for DMD patients. CHP also attenuated muscle atrophy and functional deterioration in a mouse model of age-related sarcopenia. These findings from two different models of muscle dysfunction hence warrant further investigation into the effects of CHP on muscle pathologies in animal models and eventually in patients.
在遗传性肌病中,这是一组以骨骼肌结构和代谢受损为特征的肌肉疾病,杜氏肌营养不良症(DMD)因其毁灭性的进展而引人注目。DMD的发病机制是由肌纤维的进行性退化驱动的,导致炎症和纤维化,最终影响整体肌肉生物力学。在肌肉疾病谱的另一端,与年龄相关的肌肉减少症是一种常见病症,影响着越来越多的老年人。尽管DMD和肌肉减少症具有不同的病理机制,但它们都存在进行性肌肉无力和组织炎症的发展。在此,评估了环组氨酸 - 脯氨酸(CHP)对DMD和肌肉减少症的治疗效果。在DMD的mdx小鼠模型中,结果表明CHP恢复了肌肉收缩力和力量产生,同时伴随着骨骼肌纤维化和炎症的减轻。CHP还预防了膈肌心肌病和纤维化的发展,这是DMD患者的两个主要死因。CHP还减轻了与年龄相关的肌肉减少症小鼠模型中的肌肉萎缩和功能恶化。因此,来自两种不同肌肉功能障碍模型的这些发现值得进一步研究CHP在动物模型以及最终在患者中对肌肉病理的影响。