Hongmou Zhao

Tissue engineering holds great potential for tissue repair and rejuvenation. Plant-derived exosome-like nanoparticles (ELNs) have recently emerged as a promising avenue in tissue engineering. However, there is an urgent need to understand how plant ELNs can be therapeutically applied in clinical disease management, especially for tissue regeneration. In this review, we comprehensively examine the properties, characteristics, and isolation techniques of plant ELNs. We also discuss their impact on the immune system, compatibility with the human body, and their role in tissue regeneration. To ensure the suitability of plant ELNs for tissue engineering, we explore various engineering and modification strategies. Additionally, we provide insights into the progress of commercialization and industrial perspectives on plant ELNs. This review aims to highlight the potential of plant ELNs in regenerative medicine by exploring the current research landscape and key findings.

Bioprinting is an advanced technology that allows for the precise placement of cells and biomaterials in a controlled manner, making significant contributions in regenerative medicine. Notably, bioprinting-enabled biomaterials have found extensive application as drug delivery systems (DDS) in the treatment of osteoarthritis (OA). Despite the widespread utilization of these biomaterials, there has been limited comprehensive research summarizing the recent advances in this area. Therefore, this review aims to explore the noteworthy developments and challenges associated with utilizing bioprinting-enabled biomaterials as effective DDS for the treatment of OA. To begin, we provide an overview of the complex pathophysiology of OA, highlighting the shortcomings of current treatment modalities. Following this, we conduct a detailed examination of various bioprinting technologies and discuss the wide range of biomaterials employed in DDS applications for OA therapy. Finally, by placing emphasis on their transformative potential, we discuss the incorporation of crucial cellular components such as chondrocytes and mesenchymal stem cells into bioprinted constructs, which play a pivotal role in promoting tissue regeneration and repair.

Charcot neuroarthropathy (CN) is a chronic, destructive, and painless damage of the skeletal system that affects the life quality of patients. CN, with an unclear mechanism, is characterized with invasive destruction of bones and a serious abnormality of bone metabolism. Unfortunately, development of an effective prevention and treatment strategy for CN is still a great challenge. Of note, recent studies providing an insight into the molecular mechanisms of bone metabolism and homeostasis have propelled development of novel CN therapeutic strategies. Therefore, this review aims to shed light on the pathogenesis, diagnosis, and treatment of CN. In particular, we highlight the eminent role of the osteoprotegerin (OPG)-receptor activator of nuclear factor-κB (RANK)-RANK ligand (RANKL) system in the development of CN. Furthermore, we summarize and discuss the diagnostic biomarkers of CN as well as the potential pharmacological mechanisms of current treatment regimens from the perspective of bone metabolism. We believe that this review will enhance the current state of knowledge on the diagnosis, prevention, and therapeutic efficacy of CN.

With the markedly increased diagnosis and incidence of cancer in the population, tumor bone metastasis has become a frequent event in tumor patients. Healthy bone integrity is maintained by a delicate balance between bone formation and bone resorption. Unfortunately, many tumors, such as prostate and breast, often metastasize to the bone, and the alterations to the bone homeostasis can particularly favor tumor homing and consequent osteolytic or osteoblastic lesions. Receptor activator of NF-κB ligand (RANKL), its receptor RANK, and osteoprotegerin (OPG) are involved in the regulation of the activation, differentiation, and survival of osteoclasts, which play critical roles in bone metastasis formation. High rates of osteoclastic bone resorption significantly increase fracture risk, cause severe bone pain, and contribute to homing tumor cells in bone and bone marrow. Consequently, suppression of the RANK/RANKL/OPG system and osteoclastic activity can not only ameliorate bone resorption but may also prevent tumor bone metastases. This review summarizes the important role of the RANK/RANKL/OPG system and osteoclasts in bone homeostasis and its effect on tumor bone metastasis and discusses therapeutic strategies based on RANKL inhibition.

Rheumatoid arthritis (RA) has a high incidence and adverse effects on patients, thus posing a serious threat to people’s life and health. However, the underlying mechanisms regarding the development of RA are still elusive. Herein, we aimed to evaluate the RA-associated molecular mechanisms using the scRNA-seq technique. We used the GEO database to obtain scRNA-seq datasets for synovial fibroblasts (SFs) from RA cases, and the genes were then analyzed using principal component analysis (PCA) and T-Stochastic Neighbor Embedding (TSNE) analyses. Bioinformatics evaluations were carried out for asserting the highly enriched signaling pathways linked to the marker genes, and the key genes related to RA initiation were further identified. According to the obtained results, 3 cell types (0, 1, and 2) were identified by TSNE and some marker genes were statistically upregulated in cell type 1 than the other cell types. These marker genes predominantly contributed to extracellular matrix (ECM) architecture, collagen-harboring ECM, and ECM structural components, and identified as enriched with PI3K/AKT signaling cascade. Notably, fibronectin-1 (FN-1) has been identified as a critical gene that is strongly linked to the development of SFs and has enormous promise for regulating the onset of RA. Moreover, such an investigation offers novel perspectives within onset/progression of RA, suggesting that FN-1 may be a key therapeutic target for RA therapies.

Bone and tissue degeneration are the most common skeletal disorders that seriously affect people’s quality of life. N6-methyladenosine (m6A) is one of the most common RNA modifications in eukaryotic cells, affecting the alternative splicing, translation, stability and degradation of mRNA. Interestingly, increasing number of evidences have indicated that m6A modification could modulate the expression of autophagy-related (ATG) genes and promote autophagy in the cells. Autophagy is an important process regulating intracellular turnover and is evolutionarily conserved in eukaryotes. Abnormal autophagy results in a variety of diseases, including cardiomyopathy, degenerative disorders, and inflammation. Thus, the interaction between m6A modification and autophagy plays a prominent role in the onset and progression of bone and tissue degeneration. In this review, we summarize the current knowledge related to the effect of m6A modification on autophagy, and introduce the role of the crosstalk between m6A modification and autophagy in bone and tissue degeneration. An in-depth knowledge of the above crosstalk may help to improve our understanding of their effects on bone and tissue degeneration and provide novel insights for the future therapeutics.