Charming Micro-Insights into Health and Diseases

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 30 June 2025 | Viewed by 6693

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Special Issue Information

Dear Colleagues,

The 3rd International Online Conference on Cells: Charming Micro-Insights into Health and Diseases (Cells2025) (https://sciforum.net/event/CELLS2025) was organized by the MDPI open access journal Cells (Impact Factor 6.0) and will be held online from 25 to 27 March 2025. This conference aims to provide leading scientists working in the field with an online platform on which to share their latest research and engage in exciting discussions. The main topics of the conference are as follows:

  •     Cellular pathology of cancers;
  •     Neural cell biology;
  •     Cellular antivirus immune responses;
  •     Cell therapies;
  •     Cellular signaling;
  •     Cell research in animal models;
  •     Cellular metabolism;
  •     Protein quality control;
  •     Proteasomal degradation and autophagy.

This Special Issue intends to collect the extended and expanded versions of Proceedings papers from the conference. All conference participants will be granted a 10% discount on Article Processing Charges (APCs).

Prof. Dr. Alexander E. Kalyuzhny
Guest Editor

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Keywords

  • cellular pathology of cancers
  • neural cell biology
  • cellular antivirus immune responses
  • cell therapies
  • cellular signaling
  • cell research in animal models
  • cellular metabolism
  • protein quality control
  • proteasomal degradation and autophagy

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Published Papers (4 papers)

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Research

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13 pages, 3574 KiB  
Article
The Sensory Input from the External Cuneate Nucleus and Central Cervical Nucleus to the Cerebellum Refines Forelimb Movements
by Chidubem Eneanya and George M. Smith
Cells 2025, 14(8), 589; https://doi.org/10.3390/cells14080589 - 13 Apr 2025
Viewed by 337
Abstract
Goal-directed reaching movements are extremely accurate to the point that the location, placement, and speed of the limbs are specific from trial to trial. These movements require descending motor commands and feedback modulation from ascending sensory information. The descending motor commands and ascending [...] Read more.
Goal-directed reaching movements are extremely accurate to the point that the location, placement, and speed of the limbs are specific from trial to trial. These movements require descending motor commands and feedback modulation from ascending sensory information. The descending motor commands and ascending sensory information work in conjunction to ensure that the movement is accurate and precise through an error-corrected process that resides in the cerebellum. Disruptions to this information may cause errors in the precision of forelimb motor targeting. According to the previous literature, the external cuneate nucleus (ECN) and central cervical nucleus (CeCv) are responsible for conveying unconscious sensory information from the forelimbs, shoulders, and neck muscles to the cerebellum. Here, we examined the significance of the ECN and CeCv, separately, in forelimb function. In conjunction with inhibitory DREADDs (hM4Di), we observed an obstruction in single pellet reaching and grasping when ECN activity was repressed, both unilaterally and bilaterally, in normal rats. We also observed reduced reach in the grooming assessment bilaterally. We discovered that the CeCv terminates in the medial cerebellar nucleus (MCN), within the deep cerebellar nuclei (DCN), which, to the best of our knowledge, was previously not clearly defined. Together, this information provides evidence that the requirement of ascending sensory information is important in forelimb function. Full article
(This article belongs to the Special Issue Charming Micro-Insights into Health and Diseases)
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17 pages, 4732 KiB  
Article
Anti-Inflammatory Effects of Cannabigerol In Vitro and In Vivo Are Mediated Through the JAK/STAT/NFκB Signaling Pathway
by Ga Hee Jeong, Ki Chan Kim and Ji Hyun Lee
Cells 2025, 14(2), 83; https://doi.org/10.3390/cells14020083 - 9 Jan 2025
Cited by 2 | Viewed by 3936
Abstract
Cannabinoid compounds have potential as treatments for a variety of conditions, with cannabigerol (CBG) being known for its anti-inflammatory properties. In this study, we investigated the effects of CBG in a cellular model of 1-chloro-2,4-dinitrobenzene (DNCB)-induced atopic dermatitis (AD). In the cellular model, [...] Read more.
Cannabinoid compounds have potential as treatments for a variety of conditions, with cannabigerol (CBG) being known for its anti-inflammatory properties. In this study, we investigated the effects of CBG in a cellular model of 1-chloro-2,4-dinitrobenzene (DNCB)-induced atopic dermatitis (AD). In the cellular model, we confirmed the cytotoxicity of CBG and downregulated the expression of inflammatory markers CCL26, IL1B, IL6, and TNF (p < 0.001). In the mouse model, clinical, histological, and immunological changes were analyzed. The results showed that CBG improved dermatitis severity score, epidermal thickness, and mast cell count and reduced inflammatory cytokines (Tslp, Il1b, Il4, Il6, Il13, Il17, Il18, Il22, and Il33) by qRT-PCR (p < 0.001). Western blot results showed modulated changes in JAK1, JAK2, TYK2, STAT1, STAT2, STAT3, p-STAT3, STAT6, and p-STAT6 (p < 0.05). Subsequently, p-IκBα, NF-κB, and p-NF-κB signaling factors were also reduced (p < 0.05), with corresponding changes in skin barrier factors. The results of this study indicate that CBG effectively alleviates AD-like symptoms and suggest the potential of CBG as a therapeutic agent. Full article
(This article belongs to the Special Issue Charming Micro-Insights into Health and Diseases)
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12 pages, 2056 KiB  
Communication
NLRX1 Mediates the Disruption of Intestinal Mucosal Function Caused by Porcine Astrovirus Infection via the Extracellular Regulated Protein Kinases/Myosin Light–Chain Kinase (ERK/MLCK) Pathway
by Jie Tao, Jinghua Cheng, Ying Shi, Benqiang Li, Pan Tang, Jiajie Jiao and Huili Liu
Cells 2024, 13(11), 913; https://doi.org/10.3390/cells13110913 - 25 May 2024
Viewed by 1668
Abstract
Porcine astrovirus (PAstV) has a potential zoonotic risk, with a high proportion of co-infection occurring with porcine epidemic diarrhea virus (PEDV) and other diarrheal pathogens. Despite its high prevalence, the cellular mechanism of PAstV pathogenesis is ill–defined. Previous proteomics [...] Read more.
Porcine astrovirus (PAstV) has a potential zoonotic risk, with a high proportion of co-infection occurring with porcine epidemic diarrhea virus (PEDV) and other diarrheal pathogens. Despite its high prevalence, the cellular mechanism of PAstV pathogenesis is ill–defined. Previous proteomics analyses have revealed that the differentially expressed protein NOD–like receptor X1 (NLRX1) located in the mitochondria participates in several important antiviral signaling pathways in PAstV–4 infection, which are closely related to mitophagy. In this study, we confirmed that PAstV–4 infection significantly up-regulated NLRX1 and mitophagy in Caco–2 cells, while the silencing of NLRX1 or the treatment of mitophagy inhibitor 3–MA inhibited PAstV–4 replication. Additionally, PAstV–4 infection triggered the activation of the extracellular regulated protein kinases/ myosin light-chain kinase (ERK/MLCK) pathway, followed by the down-regulation of tight–junction proteins (occludin and ZO–1) as well as MUC–2 expression. The silencing of NLRX1 or the treatment of 3–MA inhibited myosin light-chain (MLC) phosphorylation and up-regulated occludin and ZO–1 proteins. Treatment of the ERK inhibitor PD98059 also inhibited MLC phosphorylation, while MLCK inhibitor ML-7 mitigated the down-regulation of mucosa-related protein expression induced by PAstV–4 infection. Yet, adding PD98059 or ML–7 did not affect NLRX1 expression. In summary, this study preliminarily explains that NLRX1 plays an important role in the disruption of intestinal mucosal function triggered by PAstV–4 infection via the ERK/MLC pathway. It will be helpful for further antiviral drug target screening and disease therapy. Full article
(This article belongs to the Special Issue Charming Micro-Insights into Health and Diseases)
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Review

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17 pages, 955 KiB  
Review
Targeted Redox Regulation α-Ketoglutarate Dehydrogenase Complex for the Treatment of Human Diseases
by Ryan J. Mailloux
Cells 2025, 14(9), 653; https://doi.org/10.3390/cells14090653 (registering DOI) - 29 Apr 2025
Abstract
α-ketoglutarate dehydrogenase complex (KGDHc) is a crucial enzyme in the tricarboxylic acid (TCA) cycle that intersects monosaccharides, amino acids, and fatty acid catabolism with oxidative phosphorylation (OxPhos). A key feature of KGDHc is its ability to sense changes in the redox environment through [...] Read more.
α-ketoglutarate dehydrogenase complex (KGDHc) is a crucial enzyme in the tricarboxylic acid (TCA) cycle that intersects monosaccharides, amino acids, and fatty acid catabolism with oxidative phosphorylation (OxPhos). A key feature of KGDHc is its ability to sense changes in the redox environment through the reversible oxidation of the vicinal lipoic acid thiols of its dihydrolipoamide succinyltransferase (DLST; E2) subunit, which controls its activity and, by extension, OxPhos. This characteristic inculcates KGDHc with redox regulatory properties for the modulation of metabolism and mediating of intra- and intercellular signals. The innate capacity of KGDHc to participate in the regulation of cell redox homeodynamics also occurs through the production of mitochondrial hydrogen peroxide (mtH2O2), which is generated by the dihydrolipoamide dehydrogenase (DLD; E3) downstream from the E2 subunit. Reversible covalent redox modification of the E2 subunit controls this mtH2O2 production by KGDHc, which not only protects from oxidative distress but also modulates oxidative eustress pathways. The importance of KGDHc in modulating redox homeodynamics is underscored by the pathogenesis of neurological and metabolic disorders that occur due to the hyper-generation of mtH2O2 by this enzyme complex. This also implies that the targeted redox modification of the E2 subunit could be a potential therapeutic strategy for limiting the oxidative distress triggered by KGDHc mtH2O2 hyper-generation. In this short article, I will discuss recent findings demonstrating KGDHc is a potent mtH2O2 source that can trigger the manifestation of several neurological and metabolic diseases, including non-alcoholic fatty liver disease (NAFLD), inflammation, and cancer, and the targeted redox modification of the E2 subunit could alleviate these syndromes. Full article
(This article belongs to the Special Issue Charming Micro-Insights into Health and Diseases)
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