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Amidst the framework of dual circulation, innovation emerges as a pivotal strategy for realizing high-quality economic development. Concurrently, digital finance, serving as a potent complement to traditional financial systems, significantly influences regional innovation enhancement. This research employs a spatial panel methodology to thoroughly investigate the inherent mechanisms through which digital finance development shapes regional innovation. Empirical testing is conducted using panel data derived from 283 mainland Chinese prefecture-level cities spanning from 2013 to 2020. The findings underscore that digital inclusive finance plays a crucial role in amplifying regional innovation output, unveiling a distinct spatial impact on innovation. The progression of each facet of digital finance contributes to mitigating supply-side financing constraints, thereby directly fostering heightened regional innovation. The study delves into a Chinese regional sub-sample, revealing a prevalent driving effect with conspicuous heterogeneity across the major regions--East. Central. West. As scientific and technological innovation stands as the primary driving force, its profound interplay with the evolution of financial inclusion in China is evident. This study provides valuable insights to fortify regional modernization efforts and serves as a reference for policymakers and researchers navigating the complex intersection of finance and innovation in the Chinese context. [ABSTRACT FROM AUTHOR]

Background: Dedifferentiation of muscle cells in the tissue of mammals has yet to be observed. One of the challenges facing the study of skeletal muscle cell dedifferentiation is the availability of a reliable model that can confidentially distinguish differentiated cell populations of myotubes and non-fused mononuclear cells, including stem cells that can coexist within the population of cells being studied. Methodology/Principal Findings: In the current study, we created a Cre/Lox-β-galactosidase system, which can specifically tag differentiated multinuclear myotubes and myotube-generated mononuclear cells based on the activation of the marker gene, β-galactosidase. By using this system in an adult mouse model, we found that β-galactosidase positive mononuclear cells were generated from β-galactosidase positive multinuclear myofibers upon muscle injury. We also demonstrated that these mononuclear cells can develop into a variety of different muscle cell lineages, i.e., myoblasts, satellite cells, and muscle derived stem cells. Conclusions/Significance: These novel findings demonstrated, for the first time, that cellular dedifferentiation of skeletal muscle cells actually occurs in mammalian skeletal muscle following traumatic injury in vivo. [ABSTRACT FROM AUTHOR]

The decline of muscle regenerative potential with age has been attributed to a diminished responsiveness of muscle progenitor cells (MPCs). Heterochronic parabiosis has been used as a model to study the effects of aging on stem cells and their niches. These studies have demonstrated that, by exposing old mice to a young systemic environment, aged progenitor cells can be rejuvenated. One interesting idea is that pregnancy represents a unique biological model of a naturally shared circulatory system between developing and mature organisms. To test this hypothesis, we evaluated the muscle regeneration potential of pregnant mice using a cardiotoxin (CTX) injury mouse model. Our results indicate that the pregnant mice demonstrate accelerated muscle healing compared to nonpregnant control mice following muscle injury based on improved muscle histology, superior muscle regeneration, and a reduction in inflammation and necrosis. Additionally, we found that MPCs isolated from pregnant mice display a significant improvement of myogenic differentiation capacity in vitro and muscle regeneration in vivo when compared to the MPCs from nonpregnant mice. Furthermore, MPCs from nonpregnant mice display enhanced myogenic capacity when cultured in the presence of serum obtained from pregnant mice. Our proteomics data from these studies provides potential therapeutic targets to enhance the myogenic potential of progenitor cells and muscle repair. [ABSTRACT FROM AUTHOR]

Although the mouse strain Murphy Roths Large (MRL/MpJ) possesses high regenerative potential, the mechanism of tissue regeneration, including skeletal muscle, in MRL/MpJ mice after injury is still unclear. Our previous studies have shown that muscle-derived stem/progenitor cell (MDSPC) function is significantly enhanced in MRL/MpJ mice when compared with MDSPCs isolated from age-matched wild-type (WT) mice. Using mass spectrometry-based proteomic analysis, we identified increased expression of hypoxia-inducible factor (HIF) 1α target genes (expression of glycolytic factors and antioxidants) in sera from MRL/MpJ mice compared with WT mice. Therefore, we hypothesized that HIF-1α promotes the high muscle healing capacity of MRL/MpJ mice by increasing the potency of MDSPCs. We demonstrated that treating MRL/MpJ MDSPCs with dimethyloxalylglycine and CoCl2 increased the expression of HIF-1α and target genes, including angiogenic and cell survival genes. We also observed that HIF-1α activated the expression of paired box (Pax)7 through direct interaction with the Pax7 promoter. Furthermore, we also observed a higher myogenic potential of MDSPCs derived from prolyl hydroxylase (Phd) 3-knockout (Phd3-/-) mice, which displayed higher stability of HIF-1α. Taken together, our findings suggest that HIF-1α is a major determinant in the increased MDSPC function of MRL/MpJ mice through enhancement of cell survival, proliferation, and myogenic differentiation.--Sinha, K. M., Tseng, C., Guo, P., Lu, A., Pan, H., Gao, X., Andrews, R., Eltzschig, H., Huard, J. Hypoxia-inducible factor 1α (HIF-1α) is a major determinant in the enhanced function of muscle-derived progenitors from MRL/MpJ mice. [ABSTRACT FROM AUTHOR]

Three-dimensional (3D) engineered tissue constructs are a novel and promising approach to tissue repair and regeneration. 3D tissue constructs have the ability to restore form and function to damaged soft tissue unlike previous methods, such as plastic surgery, which are able to restore only form, leaving the function of the soft tissue often compromised. In this study, we seeded murinemyoblasts (C2C12) into a collagen composite scaffold and cultured the scaffold in a roller bottle cell culture system in order to create a 3D tissue graft in vitro. The 3D graft created in vitro was then utilized to investigate muscle tissue repair in vivo. The 3D muscle grafts were implanted into defect sites created in the skeletal muscles in mice. We detected that the scaffolds degraded slowly over time, and muscle healing was improved which was shown by an increased quantity of innervated and vascularized regenerated muscle fibers. Our results suggest that the collagen composite scaffold seeded with myoblasts can create a 3D muscle graft in vitro that can be employed for defect muscle tissue repair in vivo. [ABSTRACT FROM AUTHOR]