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Cells

Cells is an international, peer-reviewed, open access journal on cell biology, molecular biology, and biophysics, published semimonthly online by MDPI.
The Nordic Autophagy Society (NAS) and the Spanish Society of Hematology and Hemotherapy (SEHH) are affiliated with Cells and their members receive discounts on the article processing charges.
Indexed in PubMed | Quartile Ranking JCR - Q2 (Cell Biology)

All Articles (19,956)

Mouse models of genetic diseases are important research tools. However, the genetic background of the mouse strain can significantly influence how a genetic mutation is expressed. Studies on preclinical models of phenylketonuria (PKU), an inherited metabolic disorder, have used two strains, BTBR and C57Bl/6, created via a chemically induced point mutation in the gene encoding the enzyme phenylalanine hydroxylase (BTBRenu2 and C57enu2, respectively). Despite having the same levels of hyperphenylalaninemia (HPA), published results indicate differences in neural and behavioral phenotypes between the two backgrounds. To explore this difference further, the current study examines the genome-wide transcriptome of the prefrontal cortex (pFC), the brain region which is the most vulnerable to the negative effects of HPA. Regardless of the strain, the enu2 mutation upregulated the expression of several aminoacyl-tRNA synthetases and eukaryotic translation initiation factors, suggesting an essential modification in the protein translation process and supporting the downregulation of gene programs related to myelination. Accordingly, we deepened the exploration of cognitive dysfunctions in C57enu2− mice, showing a previously unreported working memory impairment under increasing information load. These findings identify convergent pFC molecular and cognitive alterations induced by HPA across distinct genetic backgrounds, providing clinically relevant insights into mechanisms that may contribute to executive dysfunctions in PKU.

24 January 2026

Transcriptomic analysis reveals a conserved set of differentially expressed genes (DEGs) between C57enu2 and BTBRenu2 mice. (A) Experimental plan and Venn diagram showing the overlap between DEGs identified in C57 (n = 391) and BTBR (n = 306) mice. DEGs were defined using an FDR-corrected p-value (Padj < 0.05). (B) Heatmap of the 62 overlapping DEGs between enu2 mutations on C57 and BTBR backgrounds. Genes are ordered by hierarchical clustering. Blue indicates downregulation and orange indicates upregulation relative to WT controls. While most genes are regulated similarly in both strains, Nup62, Psph, and Arhgef2 are regulated in opposite directions.

Tunneling nanotubes (TNTs) are thin, actin-based intercellular bridges that enable long-range communication during cellular stress; yet the molecular pathway controlling their formation remains unclear. Here, using gain- and loss-of-function approaches in Cath. a-differentiated (CAD) neuronal cells, we identified a unidirectional regulatory pathway in which myosin-X (Myo10) functions upstream of the actin-bundling protein L-(LCP1) to drive TNT formation. Using Western blotting and fluorescence microscopy, we determined that overexpression of L-plastin significantly increased the proportion of TNT-connected cells, whereas L-plastin downregulation reduced TNT formation, demonstrating that L-plastin is both sufficient and necessary for maintaining normal TNT abundance. Having previously shown that Myo10 is required for TNT formation in CAD cells, we asked whether the relationship is reciprocal. Overexpression/downregulation of L-plastin had no effect on Myo10 protein levels. Conversely, Myo10 downregulation decreased endogenous L-plastin by ~30%, and Myo10 overexpression elevated L-plastin expression and TNT number, demonstrating that Myo10 acts as an upstream regulator of L-plastin. Dual-color 3D imaging revealed co-localization of Myo10 and L-plastin along TNT shafts and filopodia-like precursors (Proto-TNTs). Together, these findings demonstrate that Myo10-dependent TNT formation requires the bundling protein L-plastin, providing a framework for how stress-induced signaling cascades couple TNT initiation to actin-core stabilization during stress and disease.

24 January 2026

L-plastin localizes within TNTs and proto-TNTs in CAD cells treated with hydrogen peroxide. CAD cells were treated with 100 μM H2O2 for 5 min to increase the number of TNTs between cells, fixed and labeled with anti-L-plastin antibody (red) and the membrane dye WGA-green to identify cellular protrusions (green). (a) A confocal microscopy 3D representative image of CAD cells connected with TNTs (white arrows). (b) 3D reconstruction image using Imaris software, employing “spot rendering” to identify L-plastin localization (red) within TNTs and along proto-TNTs. (c) 3D reconstruction image using Imaris software, employing “spot rendering” plus “filament tracer” to enhance the visualization of L-plastin puncta (in red) within TNTs (gray). (d) Zoom in of the 3D reconstruction using filament tracer and spot rendering in (c). All scale bars are 2 μm in length.

Despite tremendous scientific efforts aimed at glioblastoma’s (GB) ability to escape therapeutic attempts, the concern remains unsolved. Postbiotics, metabolites, and macromolecules of probiotic bacteria could become adjuvant therapeutics both dealing with cellular events constituting tumor therapy escape mechanisms and protecting normal cells from therapy-induced damage. The study aims to evaluate the dual potential of postbiotics obtained from lactic acid bacteria, L. plantarum and L. rhamnosus, on patient-derived and commercially available GB and normal cells alone and in combination with chemotherapeutic and irradiation oncotreatment regimens. Postbiotic mixtures (PMs) show cytoprotective potential against a new anti-cancer agent—ARA12—on astrocytes and cytoprotective action to irradiated normal fibroblast cells. Although GB cells’ apoptotic response varied between patient-derived cells, both PMs exert cytotoxic or cytostatic effects alone and, in most of the studied therapeutic combinations, on all tested GB cell lines. In particular, L. plantarum PM alleviates treatment escape, possibly shifting the tumor drug response from senescence to apoptosis. The results suggest that postbiotic-based adjunctive treatment could potentiate the therapeutic effect toward neoplastic cells, while alleviating chemotherapy’s adverse effects, helping clinicians to tackle the issue of therapy resistance and improve patients’ comfort.

24 January 2026

Concentration-dependent influence of PMs on viability of GB and non-neoplastic cell lines. (a) The response of U87MG cells to 72 h incubation with increasing concentrations (v/v) of L. plantarum- and L. rhamnosus-derived PMs based on resazurin viability assay PrestoBlue. Statistically significant differences in cell viability compared to untreated control are indicated by * for PM derived from L. plantarum and ** for L. rhamnosus. (b) The response of the U87MG GB cell line and normal cell lines: NHA and WI-38 treated with 30% PM (v/v) derived from L. plantarum and L. rhamnosus for 72 h. Viability was assessed by PrestoBlue assay and the presented percentage viability is normalized to the untreated control for each cell line. Statistically significant differences between U87MG and normal cell lines’ responses to PM application were marked with * for L. plantarum and ** for L. rhamnosus; (p < 0.05). PM—postbiotic mixture.

Interleukin-6 in Natural and Pathophysiological Kidney Aging

  • Kerim Mutig,
  • Prim B. Singh and
  • Svetlana Lebedeva

Kidney aging is receiving growing attention in middle- to high-income societies due to increasing longevity in general population. Chronic Kidney Disease (CKD) has been widely accepted as a major non-communicable human disease affecting over 10% of the adult population in industrialized countries. CKD is mainly caused by metabolic and cardiovascular disorders such as diabetes mellitus and hypertension, disproportionally affecting older people, whereas natural kidney aging is driven by age-dependent systemic and renal low-grade inflammation. Interleukin-6 (IL-6) is the key cytokine mediating age-related inflammation. At the same time, IL-6 has been implicated in the pathophysiology of cardiovascular and renal disorders as a major pro-inflammatory cytokine. Thereby, IL-6 is placed at the intersection between natural and pathophysiological kidney aging, and the latter accelerates systemic aging and substantially limits life quality and expectancy. Growing clinical availability of IL-6 inhibitors for treatment of autoimmune and autoinflammatory disorders demands clarification of potential renal consequences as well. Available data suggests that IL-6 inhibition may be renoprotective in some kidney disorders, but the setting of kidney aging has received only minor attention. The present review focuses on the known effects of IL-6 associated with natural or pathophysiological renal aging.

24 January 2026

Vicious circle of pathophysiological events driving renal and systemic aging.

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Cells - ISSN 2073-4409