Browsing by Subject "Muscle atrophy"

Now showing 1 - 2 of 2
  • Thumbnail Image
    Publication
    Open Access
    Disorganization of honey-comb immunoreactive pattern of desmin and plectin in rat atrophic soleus muscle fiber induced by hindlimb suspension
    (Murcia : F. Hernández, 2002) Nara, S.; Hachisuka, K.; Furukawa, H.; Doi, Y.; Kudo, H.; Fujimoto, S.
    Immunoreactivity for desmin, plectin and a- actinin was inve s t i gated in rat atrophic soleus muscle fibers induced by hindlimb suspension between 1 and 4 weeks (hindlimb suspension group, HSG), and compared with that of the control group (CG). Some of the HSG for 4 weeks were allowed unrestricted cage activity for 2 weeks as the recovery group (RG). In the cross-sectioned muscle fibers of the CG, desmin and plectin show e d h o n ey-comb immunoreactive patterns ex t e n d i n g throughout the sarcoplasm. Superimposed images by double immunofluorescence labeling show e d overlapping of both immunoreactivities. In the longitudinally sectioned profiles, superimposed images of a-actinin and desmin were overlapped at the level of Z-discs. The focal disorganization of the above honey - comb immunoreactive patterns, followed by the reduction of the cross-sectional area (CSA) of atrophic soleus muscle fibers and the appearance of Z-streaming, uniquely arose in the HSG from the first week and extended throughout the sarcoplasm in proportion to the suspension period. Such honey-comb patterns of both desmin and plectin were already restored in the RG at 2 weeks, followed by the disappearance of Z-streaming, prior to the recovery of the CSA. These findings indicate that the disorganization of topological and structural relationships of desmin and plectin with Z-discs surrounding individual myofibrils is primarily evo ke d , which leads to Z-streaming of atrophic soleus muscle fibers, and that the restoration of the muscle activity results in an early arrangement recovery of desmin and plectin around myofibrils.
  • Thumbnail Image
    Item
    Open Access
    Muscle atrophy following anterior cruciate ligament reconstruction: A narrative review
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2026) Kaneguchi, Akinori; Ozawa, Junya; Biología Celular e Histología
    Muscle weakness is a common issue following anterior cruciate ligament (ACL) reconstruction and is closely linked to muscle atrophy. Preventing or reducing this atrophy is a key goal of rehabilitation. This review summarizes current knowledge on muscle atrophy after ACL reconstruction, including its spatial distribution, time course, underlying mechanisms, and potential interventions. Atrophy affects multiple lower limb muscles and may be influenced by the type of graft used. Tendon harvesting appears to negatively impact the muscle belly of the donor muscle, while atrophy may also occur in the contralateral limb independently of graft harvesting. Muscle atrophy is often already present before surgery and tends to worsen postoperatively. Although partial recovery may occur, long-term deficits are frequently observed. At the muscle fiber level, evidence is inconsistent regarding which fiber types are more vulnerable to atrophy. A transient shift toward faster fiber types has been reported after surgery. On the cellular and molecular level, satellite cell depletion via apoptosis may hinder muscle regrowth and thereby contribute to persistent muscle atrophy. Concurrently, increased expression of myostatin, atrogin-1, and muscle RING-finger-1, along with postoperative inflammation, may promote protein degradation, further exacerbating muscle atrophy. Rehabilitation strategies that involve early immobilization or non-weight bearing may exacerbate atrophy. Interventions such as eccentric training, neuromuscular electrical stimulation, blood flow restriction training, pharmacological agents, and nutritional support demonstrate potential, but no definitive treatment has been established. Future studies using appropriate animal models to clarify the molecular mechanisms of muscle atrophy will be crucial for developing effective therapies.