The roles of Hippo/YAP signaling pathway in physical therapy

Abstract Cellular behavior is regulated by mechanical signals within the cellular microenvironment. Additionally, changes of temperature, blood flow, and muscle contraction also affect cellular state and the development of diseases. In clinical practice, physical therapy techniques such as ultrasound, vibration, exercise, cold therapy, and hyperthermia are commonly employed to alleviate pain and treat diseases. However, the molecular mechanism about how these physiotherapy methods stimulate local tissues and control gene expression remains unknow. Fortunately, the discovery of YAP filled this gap, which has been reported has the ability to sense and convert a wide variety of mechanical signals into cell-specific programs for transcription, thereby offering a fresh perspective on the mechanisms by which physiotherapy treat different diseases. This review examines the involvement of Hippo/YAP signaling pathway in various diseases and its role in different physical therapy approaches on diseases. Furthermore, we explore the potential therapeutic implications of the Hippo/YAP signaling pathway and address the limitations and controversies surrounding its application in physiotherapy

Metabolomic Analysis on the Mechanism of Nanoselenium Biofortification Improving the Siraitia grosvenorii Nutritional and Health Value

Nanoselenium (nano-Se) foliar application is crucial for enhancing plant health. However, the mechanism by which nano-Se biofortification promotes the nutritional components of Siraitia grosvenorii remains unclear. In this study, nano-Se foliar application increased the carbohydrate and amino acid contents, including glucose (23.6%), fructose (39.7%), sucrose (60.6%), tryptophan (104.5%), glycine (85.9%), tyrosine (78.4%), phenylalanine (60.1%), glutamic acid (63.4%), and proline (52.5%). Nano-Se application enhanced apigenin (3.8 times), syringic acid (0.7 times), and 4-hydroxy-3,5-dimethoxycinnamic acid (1.4 times) of the phenylpropane biosynthesis pathways. Importantly, the SgCDS (31.1%), CYP-P450 (39.1%), and UGT (24.6%) were induced by nano-Se, which enhanced the mogroside V content (16.2%). Compared to the control, nano-Se treatment dramatically enhanced aromatic substances, including 2-butanone (51.9%), methylpropanal (146.3%), n-nonanal dimer (141.7%), pentanal (52.5%), and 2-pentanone (46.0%). In summary, nano-Se improves S. grosvenorii quality by increasing nutrients and volatile organic compounds and adjusting the phenylpropane pathway

IRF1 regulation of ZBP1 links mitochondrial DNA and chondrocyte damage in osteoarthritis

Abstract Background Z-DNA binding protein 1 (ZBP1) is a nucleic acid sensor that is involved in multiple inflammatory diseases, but whether and how it contributes to osteoarthritis (OA) are unclear. Methods Cartilage tissues were harvested from patients with OA and a murine model of OA to evaluate ZBP1 expression. Subsequently, the functional role and mechanism of ZBP1 were examined in primary chondrocytes, and the role of ZBP1 in OA was explored in mouse models. Results We showed the upregulation of ZBP1 in articular cartilage originating from OA patients and mice with OA after destabilization of the medial meniscus (DMM) surgery. Specifically, knockdown of ZBP1 alleviated chondrocyte damage and protected mice from DMM-induced OA. Mechanistically, tumor necrosis factor alpha induced ZBP1 overexpression in an interferon regulatory factor 1 (IRF1)-dependent manner and elicited the activation of ZBP1 via mitochondrial DNA (mtDNA) release and ZBP1 binding. The upregulated and activated ZBP1 could interact with receptor-interacting protein kinase 1 and activate the transforming growth factor-beta-activated kinase 1-NF-κB signaling pathway, which led to chondrocyte inflammation and extracellular matrix degradation. Moreover, inhibition of the mtDNA-IRF1-ZBP1 axis with Cyclosporine A, a blocker of mtDNA release, could delay the progression of DMM-induced OA. Conclusions Our data revealed the pathological role of the mtDNA-IRF1-ZBP1 axis in OA chondrocytes, suggesting that inhibition of this axis could be a viable therapeutic approach for OA