Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
10.5
5.2
Journals
Cells
Special Issues
Cellular Signaling Networks in Development, Homeostasis, and Disease
share announcement

Cellular Signaling Networks in Development, Homeostasis, and Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: 10 July 2026 | Viewed by 1394

Special Issue Editors

Prof. Dr. Ying Xia

E-Mail Website
Guest Editor
College of Medicine, University of Cincinnati, Cincinnati, OH 45267, USA
Interests: signal transduction; tissue morphogenesis; eye and reproductive tract development
Dr. Mei Xin

E-Mail Website
Guest Editor
Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 45229, USA
Interests: cardiovascular development and disease; cardiac regeneration; vascular remodeling and malformation
Prof. Dr. Chia-Yang Liu

E-Mail Website
Guest Editor
Department of Ophthalmology, University of Cincinnati, Cincinnati, OH 45267, USA
Interests: ocular surface; cornea; wound healing; TGF-beta

Special Issue Information

Dear Colleagues,

Cellular signaling networks orchestrate the intricate and highly specific communication that governs embryonic development and maintains tissue homeostasis. These networks integrate diverse environmental and pathological cues through fine-tuned intracellular pathways to accurately control processes such as cell proliferation, differentiation, migration, and survival. Subtle perturbations of these interconnected and context-dependent pathways can lead to a spectrum of diseases, including developmental disorders, cancer, and degenerative conditions.

This Special Issue will bring together cutting-edge research articles and comprehensive reviews designed to unravel the complexity of cellular signaling across diverse biological systems. From fundamental mechanisms that govern development processes to the context-specific pathways that maintain adult tissue homeostasis, contributions will highlight both the common principles and the unique specificity of signaling networks. This Special Issue will provide new insights into how cells communicate, adapt, and malfunction and will offer a strong foundation for advancing our mechanistic understanding and therapeutic strategies.

Prof. Dr. Ying Xia
Dr. Mei Xin
Prof. Dr. Chia-Yang Liu
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cell fate determination
  • cell migration and survival
  • cell proliferation and differentiation
  • development and homeostasis
  • developmental disorders
  • disease mechanisms
  • regenerative medicine
  • signal transduction
  • signaling crosstalk
  • spatial transcriptomics

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

19 pages, 2429 KB  
Article
Valosin-Containing Protein Contributes to Plexiform Neurofibroma Formation and Represents a Novel Therapeutic Target
by Lalitha Gopalan, Youjin Na, Liang Hu, Ashley Hall, Mi-Ok Kim, Eva Dombi, Sara Szabo, Nancy Ratner, Gang Huang and Jianqiang Wu
Cells 2026, 15(9), 848; https://doi.org/10.3390/cells15090848 - 6 May 2026
Viewed by 316
Abstract
Neurofibromatosis type 1 (NF1) patients are predisposed to develop plexiform neurofibromas (PNFs). By cross-comparison of RNA sequencing and RUNX1-CHIP sequencing data on mouse PNFs, we found that transcripts encoding the NF1-interacting p97/valosin-containing protein (VCP) gene are overexpressed in PNFs. Co-immunoprecipitation confirmed that VCP [...] Read more.
Neurofibromatosis type 1 (NF1) patients are predisposed to develop plexiform neurofibromas (PNFs). By cross-comparison of RNA sequencing and RUNX1-CHIP sequencing data on mouse PNFs, we found that transcripts encoding the NF1-interacting p97/valosin-containing protein (VCP) gene are overexpressed in PNFs. Co-immunoprecipitation confirmed that VCP bounded to neurofibromin. Western blot and immunostaining confirmed VCP overexpression in both mouse and human PNFs. Treatment of primary mouse PNF Schwann cells with CB-5083, a p97/VCP inhibitor, led to accumulation of poly-ubiquitinated proteins and generation of irresolvable proteotoxic stress. Pharmacological or genetic inhibition of VCP reduced mouse PNF cell-derived sphere number, and genetic inhibition of Vcp in Schwann cell precursors decreased tumor-like lesion numbers in a cell transplantation model. In vivo treatment with CB-5083 in Nf1fl/fl;DhhCre PNF mice significantly inhibited cell proliferation, increased cell apoptosis and reduced PNF volume. The combination with a MEK inhibitor did not increase efficacy compared to the single agent, supporting the hypothesis that VCP functions in parallel to, and may be modulated by, RAS–MAPK signaling under stress or oncogenic conditions. The significant effects of VCP inhibition in this pre-clinical study suggest a potential novel therapy for patients with PNFs. Full article
(This article belongs to the Special Issue Cellular Signaling Networks in Development, Homeostasis, and Disease)
►▼ Show Figures

Figure 1

20 pages, 2742 KB  
Article
Targeting Soluble VCAM1 and GSK3β Improves Cerebrovascular Function and Reduces Stroke Pathology in Diabetic Mice
by Masuma Akter Brishti, Mousumi Mandal, Udai Pratap Singh, Tauheed Ishrat and M. Dennis Leo
Cells 2026, 15(5), 455; https://doi.org/10.3390/cells15050455 - 4 Mar 2026
Viewed by 755
Abstract
Type 2 diabetes (T2D) features insulin resistance that promotes cerebrovascular injury, yet the immune signals linking metabolic stress to vascular dysfunction remain unclear. We tested the hypothesis that insulin resistance and soluble vascular cell adhesion molecule-1 (sVCAM1) act through complementary pathways in mast [...] Read more.
Type 2 diabetes (T2D) features insulin resistance that promotes cerebrovascular injury, yet the immune signals linking metabolic stress to vascular dysfunction remain unclear. We tested the hypothesis that insulin resistance and soluble vascular cell adhesion molecule-1 (sVCAM1) act through complementary pathways in mast cells (MCs) to raise circulating histamine levels and impair cerebral vascular function. In a high-fat diet (HFD) plus low-dose streptozotocin (STZ) model, plasma histamine rose sharply after the onset of insulin resistance and remained elevated. Plasma sVCAM1 levels also increased after insulin resistance. In vitro, recombinant sVCAM1 upregulated histidine decarboxylase (HDC) in native MCs in a dose-dependent manner, indicating a shift toward histamine synthesis, but did not enhance degranulation. In contrast, pharmacological inhibition of Akt with MK2206 activated Glycogen Synthase Kinase 3 beta (GSK3β) and increased MC degranulation without affecting HDC expression. Diabetic endothelial cell monolayers exhibited a ~twofold reduction in transendothelial electrical resistance consistent with impaired blood–brain barrier (BBB) integrity. Diabetic cerebral arteries showed receptor remodeling that favored constriction with histamine H1 receptor (H1R) expression increasing in vascular smooth muscle, while endothelial H1R and histamine H2 receptor (H2R) decreased. Functionally, insulin treatment lowered HOMA2-IR in T2D mice but did not restore cerebral artery myogenic tone or improve stroke outcomes after distal middle cerebral artery occlusion (dMCAO). Neutralizing VCAM1 with a monoclonal antibody reduced circulating sVCAM1 and histamine levels, and, together with the GSK3β inhibitor Tideglusib, stabilized MCs, normalized cerebral artery tone, and reduced post-MCAO infarct size and edema. These findings identify two distinct yet complementary mast cell pathways in T2D, highlight an immune-vascular interface that drives cerebrovascular dysfunction, and propose sVCAM1 blockade plus GSK3β inhibition as rational strategies to protect cerebral vascular function in the diabetic brain. Full article
(This article belongs to the Special Issue Cellular Signaling Networks in Development, Homeostasis, and Disease)
►▼ Show Figures

Graphical abstract

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop