时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
However, it is not described whether RA-associated sarcopenia persists once inflammation has resolved (sarcopenic imprint), or whether dipyridamole treatment initiated after inflammatory remission can restore muscle homeostasis.
方法
Serum was collected from adult arthritic K/BxN mice and pooled for experimental use.；Mice were weighed weekly and sacrificed on day 45 after serum injection.；GA, TA, white adipose tissue (WAT) and brown adipose tissue (BAT) mass were correlated to mice body weight.2.2Motor activity testsAmbulatory activity, two-limb hanging, forelimb grip strength, and rotarod tests were conducted before serum transfer and on weekly bases for six weeks, as we previously described (Marco-Bonilla et al., 2025).
核心结论
RA: Rheumatoid Arthritis; RA + Dipy: Therapeutic treatment with dipyridamole from week 4 after RA induction; GA: Gastrocnemius; TA: Tibialis Anterior; WAT: White Adipose Tissue; BAT: Brown Adipose Tissue.All these results demonstrate that our mice model replicates human sarcopenia, with loss of body weight and muscle mass.3.2Dipyridamole reverses muscle fiber atrophy, fibrosis, and myogenic dysregulation in RA mice after inflammatory remissionReduced TA mass in RA mice was associated with fiber atrophy (Figure 2A).；No differences between groups had been reported for myogenin (MyoG) and myosin heavy chain (MHC) expression in GA muscle (Figure 2D).3.3The anti-catabolic effects of dipyridamole in skeletal muscle are associated with restoration of adenosine levels, A2BR expression and AMPK signalingOur previous study demonstrated that dipyridamole counteracts muscle atrophy and inflammation through increased muscle adenosine levels.；Dipyridamole markedly reduced IgG-positive fibers in RA muscle (Figure 3G), supporting its protective effect against sarcopenic imprint damage in RA.4DiscussionPreviously, we showed that the K/BxN model develops muscle loss associated with systemic and local inflammation, and that dipyridamole reduced disease activity while exerting anabolic effects on muscle via increased adenosine availability and stimulation of A2AR and A2BR (Marco-Bonilla et al., 2025).
局限
However, it is not described whether RA-associated sarcopenia persists once inflammation has resolved (sarcopenic imprint), or whether dipyridamole treatment initiated after inflammatory remission can restore muscle homeostasis.；However, grip strength, ambulation, and hanging endurance remained reduced.；In humans, this persistent muscle deficit may contribute to the development of frailty syndrome at older ages, highlighting the importance of early therapeutic intervention during active diseases.Several limitations of the present study should be acknowledged.
对本项目的价值
中高价值：属「衰老细胞清除 / SASP 轴」方向；细胞衰老 / senolytics / SASP栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.0/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 32,367 字符，题名指纹 0.8，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：实验性类关节炎缓解后持续肌少症对双嘧达莫有应答，并伴随腺苷与 A2BR 信号恢复
- 英文标题：Persistent sarcopenia after flare remission in experimental RA responds to dipyridamole and is associated with restoration of adenosine and A2BR signaling.
- 期刊与标识：Frontiers in pharmacology · PMID 42978682 · DOI 10.3389/fphar.2026.1949677 · PMC PMC13727610