Browsing by Subject "Therapy strategy"

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    Recent insights into limb-girdle muscular dystrophy: Impacts, therapy, and challenges
    (2025) Jiang-Ling Xiao; Zhe Zhao; Heng-Yuan Liu; Chang-Fa Tang; Chen-Chen Sun; Biología Celular e Histología
    Limb-girdle muscular dystrophy (LGMD) is a genetically heterogeneous group of muscle disorders characterized by progressive muscle atrophy and loss of motor function. Over 30 subtypes have been identified and classified into two main inheritance patterns: autosomal dominant and autosomal recessive. Besides primarily affecting skeletal muscle, certain subtypes also impact the cardiac and respiratory muscles, significantly influencing disease progression and patient survival. Substantial progress has been made in understanding the pathogenic genes and molecular mechanisms of LGMD; however, developing disease-modifying therapies remains challenging due to genetic heterogeneity, limitations in gene delivery technologies, and secondary pathological complications. Current treatments are primarily supportive, focusing on symptom management and improving quality of life rather than addressing the underlying cause. This paper summarizes recent advances in LGMD pathogenesis and emerging therapeutic strategies, highlighting progress and remaining challenges in the field.
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    Traditional Chinese medicine Yiqi Huoxue recipe attenuates hepatic fibrosis via YAP/TAZ signaling
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Zhao, Wen; Zhang, Xiaoxiao; Hou, Mengmeng; Zhang, Yuguo; Tang, Yuhui; Li, Lu; Dong, Shiming; Liu, Lingdi; Zhao, Dandan; Li, Wencong; Nan, Yuemin
    Background/Aims. The Yiqi Huoxue (YQHX) recipe has been shown to attenuate liver fibrosis, but precise mechanisms have not yet been elucidated. Recently, Yes-associated protein (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) signaling has been implicated in liver fibrogenesis. This study investigated whether the YAP/TAZ signaling is involved in the therapeutic effect of YQHX on hepatic fibrosis. Materials and Methods. Wistar rats were used to generate a model of carbon tetrachloride (CCl 4)-induced liver fibrosis. Chronic hepatitis B (CHB) patients with liver fibrosis were enrolled and assigned to receive either nucleoside/nucleotide analogues (NAs) or NAs plus YQHX. Histology, immunohistochemistry, qRT-PCR, and western blotting were conducted to mechanistically assess the therapeutic effects of YQHX on liver fibrosis. Results. YQHX markedly alleviated morphological alterations in CCl 4-induced liver fibrosis and decreased markers of hepatic fibrosis in rats. Furthermore, YQHX significantly suppressed CCl 4-meidated activation of the transforming growth factor-beta (TGF-β)/Smad signaling pathway. Notably, CCl 4 induced up-regulation of YAP, TAZ, and connective tissue growth factor (CTGF), which were significantly abrogated by YQHX. Consistent with the above major findings in rats, CHB patients treated with NAs plus YQHX had greater improvement in liver fibrosis than those given NAs alone (71.4% vs. 28.6%; P=0.057). In addition, hepatic and plasma levels of YAP were significantly decreased after YQHX treatment in CHB patients with liver fibrosis. Conclusion. YAP/TAZ signaling plays a role, at least in part, in the anti-fibrotic activity of YQHX. The findings may help to better understand the mechanisms of YQHX in the treatment of liver fibrosis