Differences in lung anatomy between mice and humans, as well as frequently disappointing results when using animal models for drug discovery, emphasise the unmet need for models that can complement animal studies and improve our understanding of human lung physiology, regeneration and disease. Recent papers have highlighted the use of three-dimensional organoids and organs-on-a-chip to mimic tissue morphogenesis and function Here, we focus on the respiratory system and provide an overview of these models, which can be derived from primary lung cells and pluripotent stem cells, as well as healthy or diseased lungs. We emphasise their potential application in studies of respiratory development, regeneration and disease modelling.
Department of Integrated Traditional Chinese and Western Medicine, Xiangya Hospital, Central South University, Jiangxi Hospital, National Reginal Center for Neurological Disease, Honggutan District, No.266 Fenghe North Avenue, Nanchang, 330038, Jiangxi, China.
Acute injury and secondary injury caused by traumatic brain injury (TBI) seriously threaten the health of patients. The purpose of this study was to investigate the role of β-Asarone in TBI-induced neuroinflammation and injury. In this work, the effects of β-Asarone on nerve injury and neuronal apoptosis were investigated in mice with TBI by controlled cortical impingement.
Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) are key downstream effectors of the Hippo pathway that regulate organ size, tissue homeostasis, and cancer development. YAP/TAZ play crucial regulatory roles in organ growth, cell proliferation, cell renewal, and regeneration. Mechanistically, YAP/TAZ influence the occurrence and progression of liver regeneration (LR) through various signaling pathways, including Notch, Wnt/β-catenin, TGF-β/Smad.
Shanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Orthodontics, Stomatological Hospital and Dental School, Tongji University, Shanghai, China.
Premature accumulation of senescent cells results in tissue destruction, and it is one of the potential primary mechanisms underlying the accelerated progression of diabetes and periodontitis. However, whether this characterized phenomenon could account for periodontal pathogenesis under hyperglycemic conditions remains unclear. In this study, we assessed the senescent phenotypic changes in experimental periodontitis under hyperglycemic conditions.
This study aimed to investigate the molecular mechanisms of periodontitis and identify key immune-related biomarkers using machine learning and Mendelian randomization (MR). Differentially expressed gene (DEG) analysis was performed on periodontitis datasets GSE16134 and GSE10334 from the Gene Expression Omnibus (GEO) database, followed by weighted gene co-expression network analysis (WGCNA) to identify relevant gene modules. Various machine learning algorithms were utilized to construct predictive models, highlighting core genes, while MR assessed the causal relationships between these genes and periodontitis.
Heart failure (HF) syndrome is of great interest as an emerging epidemic. Due to the increasing elderly population worldwide, the total number of HF patients is increasing every day. This disease places a significant economic burden on the healthcare and treatment systems of developing societies, and this situation is very concerning.
