The innate immune system, as the host’s first line of defense against intruders, plays a critical role in recognizing, identifying, and reacting to a wide range of microbial intruders. There is increasing evidence that mitochondrial stress is a major initiator of innate immune responses. When mitochondria’s integrity is disrupted or dysfunction occurs, the mitochondria’s contents are released into the cytosol. These contents, like reactive oxygen species, mitochondrial DNA, and double-stranded RNA, among others, act as damage-related molecular patterns (DAMPs) that can bind to multiple innate immune sensors, particularly pattern recognition receptors, thereby leading to inflammation. To avoid the production of DAMPs, in addition to safeguarding organelles integrity and functionality, mitochondria may activate mitophagy or apoptosis. Moreover, mitochondrial components and specific metabolic regulations modify properties of innate immune cells. These include macrophages, dendritic cells, innate lymphoid cells, and so on, in steady state or in stimulation that are involved in processes ranging from the tricarboxylic acid cycle to oxidative phosphorylation and fatty acid metabolism. Here we provide a brief summary of mitochondrial DAMPs’ initiated and potentiated inflammatory response in the innate immune system. We also provide insights into how the state of activation, differentiation, and functional polarization of innate immune cells can be influenced by alteration to the metabolic pathways in mitochondria.

The pathogenesis of psoriasis, a chronic inflammatory autoimmune skin disease with a high global prevalence, remains unclear. We performed a high-resolution single-cell RNA sequencing analysis of 94,759 cells from 13 samples, including those from psoriasis model mice and wild-type mice. We presented a single-cell atlas of the skin of imiquimod-induced mice with psoriasis and WT mice, especially the heterogeneity of keratinocytes and fibroblasts. More interestingly, we discovered that special keratinocyte subtypes and fibroblast subtypes could interact with each other through epithelial–mesenchymal transition and validated the results with drug verification. Moreover, we conducted a tentative exploration of the potential pathways involved and revealed that the IL-17 signalling pathway may be the most relevant pathway. Collectively, we revealed the full-cycle landscape of key cells associated with psoriasis and provided a more comprehensive understanding of the pathogenesis of psoriasis.

Cerebral dopamine neurotrophic factor (CDNF), previously known as the conserved dopamine neurotrophic factor, belongs to the evolutionarily conserved CDNF/mesencephalic astrocyte-derived neurotrophic factor MANF family of neurotrophic factors that demonstrate neurotrophic activities in dopaminergic neurons. The function of CDNF during brain ischemia is still not known. MANF is identified as an endoplasmic reticulum (ER) stress protein; however, the role of CDNF in ER stress remains to be fully elucidated. Here, we test the neuroprotective effect of CDNF on middle cerebral artery occlusion (MCAO) rats and neurons and astrocytes treated with oxygen–glucose depletion (OGD). We also investigate the expression of CDNF in cerebral ischemia and in primary neurons treated with ER stress-inducing agents. Our results show that CDNF can significantly reduce infarct volume, reduce apoptotic cells and improve motor function in MCAO rats, while CDNF can increase the cell viability of neurons and astrocytes treated by OGD. The expression of CDNF was upregulated in the peri-infarct tissue at 2 h of ischemia/24 h reperfusion. ER stress inducer can induce CDNF expression in primary cultured neurons. Our data indicate that CDNF has neuroprotective effects on cerebral ischemia and the OGD cell model and the protective mechanism of CDNF may occur through ER stress pathways.

Neurodegenerative diseases are a class of incurable and debilitating diseases characterized by progressive degeneration and death of cells in the central nervous system. They have multiple underlying mechanisms; however, they all share common degenerative features, such as mitochondrial dysfunction. According to recent studies, neurodegenerative diseases are associated with the accumulation of dysfunctional mitochondria. Selective autophagy of mitochondria, called mitophagy, can specifically degrade excess or dysfunctional mitochondria within cells. In this review, we highlight recent findings on the role of mitophagy in neurodegenerative disorders. Multiple studies were collected, including those related to the importance of mitochondria, the mechanism of mitophagy in protecting mitochondrial health, and canonical and non-canonical pathways in mitophagy. This review elucidated the important function of mitophagy in neurodegenerative diseases, discussed the research progress of mitophagy in neurodegenerative diseases, and summarized the role of mitophagy-related proteins in neurological diseases. In addition, we also highlight pharmacological advances in neurodegeneration.

Background: The flipped classroom teaching method has been increasingly adopted in recent years for teaching clinical medical specialties in medical schools around the world. However, the outcomes of this approach have not been systematically and quantitatively assessed. This meta-analysis aims to rigorously compare the effects of flipped classroom (FC) and traditional classroom (TC) teaching models on students’ learning in clinical medicine.Methods: We conducted a systematic search for all randomized and quasi-randomized controlled trials (RCTs/Q-RCTs) comparing traditional classrooms and flipped classrooms in the context of clinical medical education. The literature search included the Cochrane Library, PubMed, Embase, and Web of Science, with the final retrieval conducted on October 26, 2024. We screened the literature based on predefined inclusion and exclusion criteria. The quality of each study was assessed using RevMan (Version 5.4). The outcome indicators included theoretical scores, composite scores, skills scores, and student satisfaction. Data extraction and subsequent meta-analysis were performed using Stata 17.0 software.Results: A total of 12 studies were included in the analysis. The meta-analysis revealed that the flipped classroom (FC) group exhibited significantly higher theoretical scores (SMD = 0.481, 95% CI: 0.214 to 0.748, p = 0.000), composite scores (SMD = 0.642, 95% CI: 0.273 to 1.011, p = 0.001), and skills scores (SMD = 0.660, 95% CI: 0.312 to 1.008, p = 0.000) compared to the traditional classroom (TC) group. However, no statistically significant difference was observed in student satisfaction (SMD = −0.195, 95% CI: −1.081 to 0.691, p = 0.667).Conclusion: The flipped classroom teaching method is more effective in enhancing the theoretical scores, composite scores, and skill scores of clinical medicine students compared to the traditional classroom teaching method. However, there was no statistically significant difference in student satisfaction between the two teaching approaches. Due to the limitations of the included studies, further robust randomized controlled trials (RCTs) across diverse educational contexts are necessary to validate these findings.