Extant research pays little attention to migrant workers’ skill accumulation/upgrading from the perspective of the labor supply. This paper takes China as an example to explore the factors influencing skill accumulation of rural-urban migrant workers (RUMWs), with a purpose to discover how to sustain or reshape regional competitive advantage through improving RUMWs’ skill accumulation. Structured questionnaire surveys were adopted for data collection in Suzhou City, Jiangsu Province and Taizhou City, Zhejiang Province located in the Yangtze River Delta in the east of China. 900 questionnaires were issued and 491 effective questionnaires were recovered totally. This paper takes a perspective of global production networks, and gets a broad viewpoint containing intra-firm coordination, inter-firm partnership and extra-firm bargaining with non-firm actors, beyond what the extant literature on laborers’ human capital focuses on. The finding indicates that firms’ skill-oriented preference, which concerns about employees’ skills and innovation ability and stimulates them to learn initiatively, have a significant influence on RUMWs’ skill accumulation. In terms of collective efficiency based on co-competitive relationship between local firms, the more intensive interactions are, the more opportunities of skill accumulation RUMWs get. The accessibility of local institutions and favorable policies benefit RUMWs’ skill accumulation. Besides, the place itself, as a synthesized space of labor-management relations inside a firm and inter-organization relations, exerts an influence on and cause the regional differences in RUMWs’ skill accumulation.

Skeletal muscle atrophy is one of the major side effects of high dose or sustained usage of glucocorticoids. Pyroptosis is a novel form of pro-inflammatory programmed cell death that may contribute to skeletal muscle injury. Trimetazidine, a well-known anti-anginal agent, can also improve skeletal muscle performance both in human and mice. We here showed that dexamethasone induced atrophy, evidenced by the increase of muscle atrophy F-box (Atrogin-1) and muscle ring finger 1 (MuRF1) expression , and the decrease of myotube diameter in C2C12 myotubes. Dexamethasone also induced pyroptosis, indicated by upregulated pyroptosis-related protein NLRP3, Caspase-1 and GSDMD. Knockdown of NLRP3 or GSDMD attenuated dexamethasone-induced myotube pyroptosis and atrophy. Trimetazidine administration ameliorated dexamethasone-induced muscle atrophy both in vivo and in vitro. Moreover, trimetazidine improved exercise tolerance, as evidenced by increased running distance and running time, as well as increased skeletal muscle mass in dexamethasone-treated mice. Mechanically, trimetazidine could reverse dexamethasone-induced activation of pyroptosis both in C2C12 myotubes and in mice. Taken together, our present study demonstrated that NLRP3/GSDMD pathway-mediated pyroptosis was involved in dexamethasone-induced skeletal muscle atrophy. Trimetazidine could partially alleviate dexamethasone-induced skeletal muscle atrophy, and increase the diameter of C2C12 myotubes via inhibiting pyroptosis. Thus, trimetazidine might be a potential therapeutic compound for the prevention of muscle atrophy in glucocorticoid-treated patients.