Objective To summarize the current status and hotspots of research on obesity and neuroinflammation in the last decade through bibliometric analysis. Method Web of Science database was searched for English literature on obesity and neuroinflammation published between 2011 and 2021. The CiteSpace software was applied to analyze the number of publications, authors, institutions, countries and collaborations, and keywords in the field of obesity and neuroinflammation research.Results A total of 548 articles were included, and the number of articles had been increasing year by year. The top three countries in the field of obesity and neuroinflammation research were the United States, China, and Brazil. University of Toronto was the core research institution. Keywords formed 16 clusters, and there were a total of 15 emergent words.Conclusions Over the past decade, research on obesity and neuroinflammation has shown an upward trend. The research hotspots in the field of obesity and neuroinflammation mainly focus on insulin resistance, obesity, Alzheimer’s disease, high fat diet, inflammation, neuroinflammation, and other aspects. The prefrontal cortex and memory impairment are future hotspots.
Ischemic stroke (IS) is one of the important diseases threatening human health. The occurrence and development of IS can trigger a series of complex pathophysiological changes, including damage to the blood-brain barrier, ion imbalance, oxidative stress, mitochondrial damage, which ultimately lead to the apoptosis and necrosis of nerve cells in the ischemic area. Impaired blood-brain barrier is a key factor for cerebral edema, hemorrhagic transformation and poor prognosis in patients with IS, and neuroinflammatory response plays an important role in the damage and repair of the blood-brain barrier. This article mainly focuses on the neuroinflammatory response mediated by glial cells, pro-inflammatory cytokines and matrix metalloproteinases and the related mechanisms of IS blood-brain barrier damage and repair, in order to provide new directions for the treatment of IS.
The degree of pain in knee osteoarthritis is often inconsistent with joint structural damage. After tissue injury, pain sensitization can occur, mediated by pro-inflammatory factors enhancing neuroinflammation and nociceptive input, which triggers significant pain. Currently, low-impact aerobic exercise can inhibit neuroinflammation and enhance descending pain inhibitory pathways, thereby reducing pain; isometric resistance training, on the other hand, reduces central sensitization effects by improving central nervous system plasticity. Both are core exercises for anti-inflammation and desensitization. This article focuses on the mechanisms of neuroinflammation, emphasizing anti-inflammation, avoiding harmful movements, and promoting descending inhibitory pathways and central plasticity. Based on this, targeted intervention programs are designed to provide basis for formulating optimal exercise strategies for patients with knee osteoarthritis.
Objective To investigate the mechanism of the mechanosensitive ion channel Piezo1 in microglial ferroptosis following spinal cord injury (SCI), and to assess the effects of Piezo1 inhibition on ameliorating the injury microenvironment and promoting neurological functional recovery. Methods Primary microglia cells were extracted from neonatal 1-2 days C57BL/6 mice and divided into control group, Yoda1 (Piezo1 agonist) group, and Yoda1+GsMTx4 (Piezo1 inhibitor) group. Live/dead cell staining, reactive oxygen species (ROS) fluorescence staining, 5, 5’, 6, 6’-tetrachloro-1, 1’, 3, 3’-tetraethylbenzimidazolylcarbocyanine iodide (JC-1) mitochondrial membrane potential detection, and transmission electron microscopy were utilized to assess microglial ferroptosis and mitochondrial functional characteristics. SPF female C57BL/6 mice aged 6 to 8 weeks were used to detect the expression of Piezo1 at different time points after SCI by Western blot, and the two time points with no significant change and the most significant change in Piezo1 expression after SCI were selected for subsequent experiments. T8, T9 SCI models were established by modified Allen’s method, and were divided into sham operation group, injury group, and injury+shPiezo1 group (Piezo1-targeted interfering virus AAV-shPiezo1 was injected in situ to knock down the expression of Piezo1 14 days before modeling). Colocalization of Piezo1 with microglial markers purinergic receptor P2Y12 (P2ry12), and the expressions of glutathione peroxidase 4 (GPX4) and acyl coenzyme A synthetase long chain member 4 (ACSL4) were observed by immunofluorescence staining. Basso Mouse Scale (BMS) score was used to assess hindlimb motor function in mice. The level of ROS was detected by dihydroethidium (DHE) staining; the content of malondialdehyde (MDA) was detected by MDA kit; the levels of tumor necrosis factor α (TNF-α) and interleukin 10 (IL-10) were detected by ELISA assay; the pathological morphology of spinal cord was observed by HE staining. Results In vitro experiments showed that compared with the control group, the Yoda1 group had typical ultrastructural changes of ferroptosis, such as increased microglial cell death, enhanced ROS fluorescence, mitochondrial membrane potential depolarization, mitochondrial shrinkage and mitochondrial cristae breakage (all P<0.05), while the GsMTx4 group could partially reverse the above effects (P<0.05). In vivo experiments demonstrated that the expression of Piezo1 in spinal cord tissue was up-regulated sequentially after SCI, and reached the peak on the 7th day after SCI (P<0.05), and it was mainly localized in P2ry12-positive microglia. Compared with the injury group, in the injury+shPiezo1 group, the expression of ferroptosis core protein GPX4 in microglia was increased, the expression of ACSL4 was decreased, the levels of ROS and MDA in spinal cord tissue were decreased (P<0.05), the level of pro-inflammatory factor TNF-α was decreased, and the level of anti-inflammatory factor IL-10 was increased (P<0.05). In addition, the BMS score was significantly higher than that of the injury group (P<0.05) from the 14th day after operation, and the spinal cord tissue structure was relatively well preserved, and the cavity area was reduced. Conclusion SCI activates the Piezo1 channel in microglia, triggering mitochondrial dysfunction and mediating cellular ferroptosis, thereby aggravating secondary neuroinflammation. Targeted inhibition of Piezo1 effectively blocks the ferroptosis process, ameliorates the immune microenvironment, and promotes tissue repair and locomotor functional recovery after SCI.