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New Insights into Intercellular Communication and Signal Transduction
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New Insights into Intercellular Communication and Signal Transduction

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 June 2026 | Viewed by 1269

Special Issue Editor

Dr. Dongki Yang

E-Mail Website
Guest Editor
Department of Physiology, College of Medicine, Gachon University, Incheon 21999, Republic of Korea
Interests: acute pancreatitis; cystic fibrosis; chronic pancreatitis; pancreatic bicarbonate secretion; salivary gland function and dysfunction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cells in our body must communicate effectively to function properly. This process, known as intercellular signaling, plays a key role in regulating essential functions such as growth, immune responses, and tissue repair. Traditionally, scientists have studied well-known signaling pathways involving hormones, neurotransmitters, and cytokines.

In recent years, however, researchers have uncovered new modes of cellular communication, including tiny vesicles called exosomes, direct connections like tunneling nanotubes, and even mechanical signals. At the same time, advanced technologies such as single-cell analysis, high-resolution imaging, and AI-powered data tools have greatly improved our ability to explore these complex interactions.

These breakthroughs not only deepen our understanding of how the body works but also open up new possibilities for diagnosing and treating conditions like cancer, autoimmune diseases, and neurological disorders.

Dr. Dongki Yang
Guest Editor

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Keywords

  • intercellular communication
  • signal transduction
  • extracellular vesicles (EVs)
  • exosomes
  • tunneling nanotubes (TNTs)
  • cytokines
  • hormonal signaling
  • neurotransmitters
  • mechanotransduction
  • immune signaling

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Published Papers (2 papers)

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Research

15 pages, 5042 KB  
Article
The Role of the HMGB1 C-Terminal Domain in Epithelial–Mesenchymal Transition and Invasion in 2D and 3D MDA-MB-231 Breast Cancer Models
by Desislava Vladimirova, Shazie Yusein-Myashkova, Evdokia Pasheva, Iva Ugrinova and Jordana Todorova
Int. J. Mol. Sci. 2026, 27(7), 3146; https://doi.org/10.3390/ijms27073146 - 30 Mar 2026
Viewed by 284
Abstract
High-mobility group box 1 (HMGB1) is a multifunctional protein that operates both within the nucleus and as an extracellular signaling molecule. Its extracellular activity has been increasingly associated with cancer progression. Emerging evidence suggests that structural modifications of HMGB1, including C-terminal truncation, may [...] Read more.
High-mobility group box 1 (HMGB1) is a multifunctional protein that operates both within the nucleus and as an extracellular signaling molecule. Its extracellular activity has been increasingly associated with cancer progression. Emerging evidence suggests that structural modifications of HMGB1, including C-terminal truncation, may alter its biological activity, though the underlying mechanisms remain largely unexplored. Here, we show that HMGB1, which lacks the entire C-terminal acidic tail, is associated with increased cellular plasticity and invasive potential through distinct signaling pathways not strictly dependent on RAGE (Receptor for Advanced Glycation End-product) under the tested conditions. Functional analyses indicate that this truncated form promotes epithelial–mesenchymal transition-related behaviors and activates downstream inflammatory signaling in a context-dependent manner. Notably, pharmacological intervention with metformin effectively suppressed responses to the full-length protein but was less effective against the tail-less variant, underscoring potential therapeutic challenges. These findings suggest an underappreciated regulatory role of the HMGB1 C-terminal domain in tumor aggressiveness. Full article
(This article belongs to the Special Issue New Insights into Intercellular Communication and Signal Transduction)
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18 pages, 8098 KB  
Article
Triamcinolone Modulates Chondrocyte Biomechanics and Calcium-Dependent Mechanosensitivity
by Chen Liang, Sina Jud, Sandra Frantz, Rosa Riester, Marina Danalache and Felix Umrath
Int. J. Mol. Sci. 2026, 27(2), 1055; https://doi.org/10.3390/ijms27021055 - 21 Jan 2026
Viewed by 432
Abstract
Glucocorticoids are widely applied intra-articularly to alleviate inflammation and pain in osteoarthritis (OA). However, repeated administration and high local concentrations can lead to crystal deposition on the cartilage surface, contributing to chondrocyte damage and extracellular matrix (ECM) degradation, potentially accelerating OA progression. Calcium-dependent [...] Read more.
Glucocorticoids are widely applied intra-articularly to alleviate inflammation and pain in osteoarthritis (OA). However, repeated administration and high local concentrations can lead to crystal deposition on the cartilage surface, contributing to chondrocyte damage and extracellular matrix (ECM) degradation, potentially accelerating OA progression. Calcium-dependent mechanosensors play a critical role in mediating catabolic responses in chondrocytes, but it remains unclear whether glucocorticoids affect chondrocyte mechanosensitivity or biomechanical properties. This in vitro study examined the dose-dependent effects of triamcinolone acetonide (TA) on chondrocyte biomechanics and mechanosensitivity. Primary human chondrocytes (N = 23) were cultured for one week with TA (2 µM–2 mM) or control medium. Cytoskeletal organization was visualized by F-actin staining (N = 6), and cellular elasticity (N = 5) was quantified via atomic force microscopy (AFM). Mechanotransduction was analyzed by Ca2+ imaging (Fluo-4 AM) upon AFM-based indentation (500 nN). Expression of matrix-related and mechanosensitive genes (N = 9) was assessed by qPCR. TA exposure induced a concentration-dependent reorganization of the F-actin cytoskeleton, pronounced at 0.2 mM, accompanied by a significant increase in the elastic modulus (p < 0.001). TA further augmented Ca2+ fluorescence intensity under basal conditions and during mechanical stimulation. Blocking cationic mechanosensitive channels with GsMtx4 (N = 3) markedly reduced the TA-evoked Ca2+ influx (p < 0.0001). Significant reduction in MMP1 was observed on the transcriptional level (N = 9) after TA-treatment (p < 0.05). In summary, TA enhances chondrocyte stiffness through cytoskeletal condensation and amplifies Ca2+-dependent mechanotransduction but reduces MMP1 expression, indicating a dual biomechanical response of chondrocytes to OA under exposure of potent corticosteroid. Full article
(This article belongs to the Special Issue New Insights into Intercellular Communication and Signal Transduction)
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