The FASEB Journal最新文献

P. Di Tomo, N. Alessio, S. Falone, et al., “Endothelial Cells From Umbilical Cord of Women Affected by Gestational Diabetes: A Suitable In Vitro Model to Study Mechanisms of Early Vascular Senescence in Diabetes,” FASEB Journal 35 (2021): e21662, https://doi.org/10.1096/fj.202002072RR.

The authors inadvertently reused and relabeled the RB panel in Figure 5C as the p16 panel in Figure 5C with a horizontal flip. The RB image has been replaced with the corrected image taken contemporaneously with the other blot images. This error does not affect the interpretation of the results or the conclusions of the study.

Additionally, the same β-actin loading control was used for Figure 1B with SOD1 as the experiment as in Figure 3B with SOD2 as the experiment, as both experiments were performed simultaneously. This reuse was not declared in the original text.

The authors apologize for the errors.

The filtration function of glomeruli requires slit diaphragms formed by interdigitating podocyte foot processes, which are actin-based membrane protrusions. Failure in the maintenance of these cytoskeletal structures leads to foot process effacement, proteinuria, and progression to chronic kidney disease. We report WNK1 kinase activity is required for normal glomerular function in vivo and test the hypothesis that WNK1 kinase activity affects the structure of podocyte foot processes through modulation of actomyosin activity and focal adhesion complexes. Perturbation of cytoskeletal structure and focal adhesion signalosomes with WNK1 kinase inhibition supports a role for WNK1 in the maintenance of podocyte foot processes and sarcomere-like structures (SLSs) that are induced in models of podocyte injury. Applicability of WNK1 kinase activity modulation toward treatment of podocyte injury was assessed using primary and immortalized podocyte cell lines developed from control and Col4a3^−/− Alport Syndrome model mice. Collectively, the results provide compelling evidence that WNK1 kinase signalosome activity, which includes regulation of nascent focal adhesion formation and NMII activity at membrane protrusions and extensions, is necessary for physiological maintenance of slit diaphragms.

X. Zhou, Q. Wu, Y. Lu, et al., "Crosstalk Between Soluble PDGF-BB and PDGFRβ Promotes Astrocytic Activation and Synaptic Recovery in the Hippocampus After Subarachnoid Hemorrhage," Faseb, 33 (2019): 9588-9601. https://doi.org/10.1096/fj.201900195R

The authors inadvertently reused and relabeled the p-STAT3 panel in Figure 4A as the p-STAT3 panel in Figure 6E. The p-STAT3 image has been replaced with the corrected image in Figure 6. This error does not affect the interpretation of the results or the conclusions.

The authors apologize for the errors.

Exosomes are naturally occurring nanovesicles present in a variety of bodily fluids that facilitate the transport of proteins and nucleic acids. Characterized by their low immunogenicity and high biocompatibility, exosomes can efficiently navigate through biological barriers. This review summarizes the applications of exosomes in disease diagnosis and treatment, emphasizing their roles as biomarkers for non-invasive detection, as well as engineered vehicles for drug delivery and vaccine development. Additionally, this review also discusses recent technological advancements in exosome engineering, including genetic modification techniques and chemical modifications aimed at optimizing targeted delivery systems and enhancing immunomodulation strategies. Notably, it highlights the significant potential of exosomes to transform non-invasive diagnostics while promoting the development of sophisticated therapeutic carriers.

Epidemiological evidence supports sex-specific prevalence patterns of respiratory disease, yet the molecular basis of these dimorphic patterns under normal physiological conditions remains poorly understood. Using an isogenic murine model, we assessed bronchial responsiveness to methacholine in male and female adult offspring, with and without maternal exposure to air pollution particulates. We confirmed that males exhibit significantly greater bronchial responsiveness than females, independent of maternal exposure. RNA sequencing of lung tissue, coupled with gene co-expression analysis, revealed differentially expressed genes and sex-specific gene network modules associated with this physiological dimorphism. Interestingly, although maternal exposure did not alter the physiological response, it did interact with sex to affect which gene modules are associated with bronchial responsiveness. These findings provide new insight into the molecular architecture of sex-based differences in lung function and highlight the importance of incorporating both sex and developmental context in respiratory research.

Recent evidence demonstrates that tau phosphorylation, traditionally viewed as a hallmark of neurodegeneration, also occurs in completely reversible physiological contexts such as mammalian hibernation and human neonatal development. These findings challenge the classical protein-centric “proteinopathy” model of Alzheimer's disease (AD) and other tauopathies. Instead, we propose that phosphorylated tau (p-tau) functions as an adaptive molecular response to metabolic or neuronal activity shifts, and that tauopathies such as AD represent a failure of broader mechanisms that normally restore tau protein homeostasis. Therapeutic strategies should focus on restoring tau protein homeostasis and functionality rather than simply removing phosphorylated species. To achieve this, we discuss one possible therapeutic strategy: dismantling aggregated tau species.