Objective To review the progress of the mechanisms of Wnt/β-catenin and nuclear factor-kappa B (NF-кB) pathways in the process of the intervertebral disc degeneration. Methods The related literature about the mechanisms of Wnt/β-catenin and NF-кB pathways in the process of the intervertebral disc degeneration was reviewed, analyzed, and summarized. Results Wnt/β-catenin and NF-кB pathways are both activated in the process of the intervertebral disc degeneration, and exist interaction. However, the specific mechanisms and interactive mediums of Wnt/β-catenin and NF-кB pathways in the process of the intervertebral disc degeneration are still unclear. Conclusion The mechanisms of Wnt/β-catenin and NF-кB pathways in the process of the intervertebral disc degeneration have to be studied deeply.
Objective To review the latest development of the research on the selfrenwal signaling pathway and culture system in vitro of the embryonic stem cells(ESCs). Methods The recent articlesabout the selfrenewal signaling pathway and culture system in vitro of the ESCs were extensively reviewed. Results Understanding of the molecular mechanism of the selfrenewalin vitro and pluripotency of the ESCs was considered important for developing improved methods of deriving, culturing and differentiating these cells into the cells that could be successfully used in the clinical practice. Conclusion A further research is needed to elucidate the selfrenewal signaling pathway and the pluripotency of the ESCs and the culture systemin vitro forthe human ESCs remains to be further improved and developed.
Extracellular vesicles (EVs), defined as cell-secreted nanoscale vesicles that carry bioactive molecules, have emerged as a promising therapeutic strategy in tumor and tissue regeneration. Their potential in repairing intervertebral disc degeneration (IDD) through multidimensional regulatory mechanisms is a rapidly advancing field of research. This paper provided an overview of the mechanisms of EVs in IDD repair, thoroughly reviewed recent literature on EVs for IDD, domestically and internationally, and summarized their therapeutic mechanisms. In IDD repair, EVs could act through different mechanisms at the molecular, cellular, and tissue levels. At the molecular level, EVs could treat IDD by inhibiting inflammatory reactions, suppressing oxidative stress, and regulating the synthesis and decomposition of extracellular matrix. At the cellular level, EVs could treat IDD by inhibiting cellular pyroptosis, ferroptosis, and apoptosis and promoting cell proliferation and differentiation. At the tissue level, EVs could treat IDD by inhibiting neovascularization. EVs have a strong potential for clinical application in the treatment of IDD and deserve more profound study.
ObjectiveTo review the mechanism and research progress of signal ing pathways which play key roles in the regulation of osteoblast differentiation and bone formation. MethodsRecent articles about signal ing pathways of osteoblast differentiation and bone formation were reviewed and comprehensively analyzed. ResultsAt present, multi ple signaling pathways have been found to be involved in the regulation of osteoblast differentiation and bone formation, among which bone morphogenetic protein-Smads, Wnt/β-catenin, Notch, Hedgehog, and fibroblast growth factor signaling pathways may play the most important roles. Not only each pathway has a complex regulatory mechanism itself, but also contacts and impacts with each other, thus they formed a more compl icated and sophisticated regulatory network, and regulate together osteoblast differentiation and bone formation. However, the mechanisms in detail of those pathways are still not very clear, because the animal experiment techniques are not yet mature as well as the relevant cl inical trials were carried out not too much. ConclusionThe complete molecular mechanism of osteoblast differentiation and bone formation should be further investigated, so as to lay a theory foundation for preventing and treating the common bone diseases in cl inical which are involve in osteoblast differentiation and bone formation.
Objective To summarize the relationship between tumor necrosis factor receptor-associated factor 6 （TRAF6） and apoptosis. Methods Domestic and international researches on progress of TRAF6 and apoptotic signaling pathway， especially focused on the functional features of TRAF6 in different system diseases were searched and reviewed. Results TRAF6 took part in several signaling pathways， which had been implicated in regulating apoptosis， and its roles differed in different system diseases and in different conditions. TRAF6 promoted tumorigenesis by inhibiting apoptosis， while it played a proapoptotic or prosurvival role in nervous system and inflammatory diseases. Conclusion TRAF6 plays an important role in apoptosis and involves in the development of tumor， nervous system disease， and inflammatory diseases.
Objective To analyze the clinical presentations and radiological characteristics of acute exacerbation of idiopathic pulmonary fibrosis ( IPF) . Methods Clinical and radiological data of 2 patients with acute exacerbation of IPF from April 2006 to July 2008 were retrospectively analyzed and literatures were reviewed. Results Both patients were senior male patients over 60 years old. Dyspnea, cough and inspiratory crackles were the major symptoms and signs. Two patients were experiencing an exacerbation of dyspnea for one week and half of month, respectively. PaO2 /FiO2 of both patients was less than225 mm Hg. In both patients, high-resolution computed tomography ( HRCT) scans at the exacerbation showed typical signs of IPF including peripheral predominant, basal predominant reticular abnormality, with honeycombing and traction bronchiectasis and bronchiolectasis, and newly developing alveolar opacity. HRCT scan showed peripheral area of ground-glass attenuation adjacent to subpleural honeycombing in one patient, and diffusely distributed ground-glass opacity in another patient. Two patients had received corticosteroid treatment. For one patient, the symptoms improved, and ground-glass attenuation adjacent to subpleural honeycombing had almostly resolved. The other patient died of respiratory failure. Conclusions Some acute exacerbation in idiopatic pulmonary fibrosis can be idiopathic. The clinical presentations mainly include the worsening of dyspnea within short time. HRCT generally demonstrates new bilateral ground-glass abnormality with or without areas of consolidation, superimposed on typical changes of IPF.
OBJECTIVE: To study the effect of overexpression of truncated type II TGF-beta receptor on transforming growth factor-beta 1(TGF-beta 1) autoproduction in normal dermal fibroblasts. METHODS: In vitro cultured dermal fibroblasts were treated with recombinant human TGF-beta 1(rhTGF-beta 1) (5 ng/ml) or recombinant adenovirus containing truncated type II TGF-beta receptor gene (50 pfu/cell). Their effects on regulating gene expression of TGF-beta 1 were observed with Northern blotting. RESULTS: rhTGF-beta 1 up-regulated the gene expression of TGF-beta 1 and type I procollagen. Overexpression of truncated receptor II down-regulated the gene expression of TGF-beta 1. CONCLUSION: Overexpression of the truncated TGF-beta receptor II decreases TGF-beta 1 autoproduction via blocking TGF-beta receptor signal. The results may provided a new strategy for scar gene therapy.
Objective To investigate the changes of respiratory mechanics in response to elevated respiratory central drive and their impacts on the inspiratory signals detection.Methods 10 normal volunteers were recruited for the study from the colleagues of the State Key Laboratory of Respiratory Disease. Rebreathing method was used to increase the end expiratory PCO2 ( PCO2 -ET) to the subject’s maximal tolerance in order to stimulate the increase of respiratory central drive. The changes of respiratory mechanics in response to elevated respiratory central drive and their impacts on the initiation signals of inspiration were observed.Results After re-breathing, the average maximal tolerated PCO2 -ET was ( 81. 2 ±6. 6) mm Hg. As the PCO2 -ET rising, electromyogram of diaphragmatic muscle ( RMSdi ) ,transdiaphragmatic pressure ( Pdi ) and tidal volume ( VT ) increased progressively while the time of respiratory cycle ( Ttot ) shorten gradually. As the PCO2 -ETlevel increased frombaseline [ PCO2 -ET( level-0) ] to the maximal level [ PCO2 -ET( level-4) ] , RMSdi increased from( 17. 17 ±12. 41) μV to ( 147. 99 ±161. 64) μV,Pdi and VT increased from ( 7. 5 ±1. 7) cmH2O and ( 0. 68 ±0. 27) L to ( 26. 13 ±11. 51) cm H2O and ( 2. 21 ±0. 37) L respectively, while Ttot shorten from ( 2. 91 ±0. 85) s to ( 1. 92 ±0. 39) s. These four parameters of respiratory mechanics, RMSdi, Pdi, VT and Ttot, were highly correlated linearly with PCO2 -ET ( r value was 0. 956, 0. 973,0. 956 and 0. 89 respectively, all P lt;0. 001) . At the start of inspiration, the first detectable signal was electromyogramof diaphragmatic muscle ( RMSdi) , followed by mouth pressure ( Pm)and inspiratory flow ( Flow) on time sequence. As the rising of PCO2 -ET, the time lag of Pmand Flow from RMSdi after the initiation of inspiration increased gradually. However, the time lag between Flow and Pm remained constant. Conclusions At the start of inspiration, the signal of RMSdi appears first as compared with Pm and Flow. As the rising of PCO2 -ET, the time lag of Pmand Flow fromRMSdi after the initiation of inspiration increased gradually, suggesting RMSdi is more sensitive inspiratory signal, which might be used for triggering of ventilator in order to improve the synchronization, especially in the situation of elevated respiratory central drive.
Objective To introduce the basic research and cl inical potential of the hair foll icle stem cells related signal transduction in prol iferation and differentiation. Methods The recent original articles about the hair foll icle stem cells were extensively reviewed. Results Many different signal pathways had been involved in the skin development and self-newals.The hair foll icle stem cells could play an important role in the skin self-renewal and regeneration which were modulated by several different signal pathways, which included bone morphogenetic protein/transforming growth factor β, Wnt, Notch and ectodysplasin A genes. Conclusion The hair foll icle stem cells may be a future approach to repair cutaneous wounds as a cell therapy．
Objective To study the leptin-mediated intracellular signal pathways and their effects on wound healing.Methods The literature was reviewed extensively, concerning the physical and chemical characters of leptin, the mechanism of its receptor action, the receptor-related intracellular signal pathways and their roles on wound healing. Results Leptin was a protein hormone expressed by ob gene with relative molecular mass 16×103, it could activate the main singal pathways such as Janus kinase/signal transducer and activator of transcription, mitogenactivated protein kinases and phosphoinositide-3-kinase pathways through binding with its specific receptor, to participate in the modulation of multiple functions including energy metabolism, weight balance and wound healing. Leptin receptors were widely distributed in various tissues, which suggest the multiple functions of leptin. Local leptin expression was increased after skin injured, and it could stimulate keratinocytes proliferation, epithelialization, fibroblast proliferation and collagen synthesis, resulting in accelarated wound repair. Leptin expression was significantly increased after mucosal injury or bacteria infections, leading to accelarated mucosal repair through modulation of mucosal glandular secretion, improvment of mucosal blood flow, and synergistic action with endothelin-1.Conclusion Leptin can promote wound healing through activating its receptor-related intracellular signal pathways.