Special Issues
Table of Content

Cell Death and Inflammation in Signaling and Diseases

Submission Deadline: 31 December 2024 (closed) View: 292

Guest Editors

Prof. Jiann-Ruey Hong, Laboratory of Molecular Virology and Biotechnology, Institute of Biotechnology, National Cheng Kung University, Tainan 701, Taiwan.

Summary

Cell death and inflammation are intricately linked processes that play pivotal roles in signaling cascades and the pathogenesis of various diseases. Understanding the molecular mechanisms underlying the interplay between cell death and inflammation is crucial for unraveling disease etiology and developing targeted therapeutic interventions. This special issue aims to bring together leading researchers to explore the complex relationships between cell death and inflammation, shedding light on signaling pathways and their implications for a spectrum of diseases.

 

Topics to be covered:

1. Mechanisms of Cell Death Signaling:

In-depth analysis of the molecular pathways regulating apoptosis, necroptosis, pyroptosis, and other forms of cell death.

The role of key signaling molecules and their crosstalk in orchestrating cell death responses.

Advances in understanding the regulatory mechanisms that dictate cell fate decisions.

2. Inflammation Signaling Pathways:

Exploration of inflammatory signaling cascades, including the role of cytokines, chemokines, and inflammasomes.

The impact of immune cell activation and the role of pattern recognition receptors in inflammation.

Insights into how dysregulated inflammatory signaling contributes to various pathological conditions.

3. Cell Death and Inflammation in Diseases:

Comprehensive reviews on the involvement of cell death and inflammation in specific diseases, such as cancer, neurodegenerative disorders, autoimmune diseases, and infectious diseases.

Identification of key molecular targets and pathways that could serve as potential therapeutic interventions.

Case studies highlighting the clinical relevance of understanding cell death and inflammation in disease progression.

4. Emerging Technologies and Experimental Models:

Cutting-edge technologies for studying cell death and inflammation, including single-cell approaches, CRISPR-based screens, and advanced imaging techniques.

Development and application of novel experimental models to better mimic disease conditions and unravel underlying mechanisms.

Integration of omics data to provide a systems-level understanding of cell death and inflammation dynamics.

5. Therapeutic Strategies and Future Directions:

Overview of current therapeutic approaches targeting cell death and inflammation in various diseases.

Identification of potential drug candidates and innovative strategies for modulating cell death and inflammation.

Future perspectives and challenges in translating basic research findings into clinical applications.

 

This special issue aims to serve as a comprehensive resource for researchers and clinicians interested in the intricate interplay between cell death and inflammation in signaling and disease. By bringing together diverse perspectives and cutting-edge research, this collection will contribute to advancing our understanding of disease mechanisms and foster the development of novel therapeutic strategies.


Keywords

Cell Death, Inflammation Signaling, Signaling Pathway, Diseases, Cutting-Edge Research, CRISPR-Based Screens, Therapeutic Strategies

Published Papers


  • Open Access

    REVIEW

    Cell Death of Tumor Melanocytes and Treatment Options

    Olga Koval, Maria Zhilnikova, Maria Balantaeva, Mikhail Biryukov, Vasiliy Atamanov
    BIOCELL, DOI:10.32604/biocell.2025.059987
    (This article belongs to the Special Issue: Cell Death and Inflammation in Signaling and Diseases)
    Abstract Melanomas are aggressive cancers, with a high rate of metastatic disease. Cutaneous (CM) and uveal (UM) melanomas are intrinsically different diseases, and most cell death inducers effective for CM do not function for UM. This is primarily due to the fact the eye is an immunologically privileged organ, and it fails to achieve the efficacy of immune checkpoint inhibitors (ICIs) comparable to that for CM. However, approaches utilizing specific melanoma-associated antigens are being developed for metastatic forms of CM and UM. The most promising to date are gp100 and tyrosinase related protein 1 (TYRP1), primarily… More >

  • Open Access

    REVIEW

    Involvement of ZBP1 in Cancer and Its Potential Therapeutic Target Effects

    Emmanuel Mago, Jiayi Xu, Dan Weng, Yan Pan
    BIOCELL, DOI:10.32604/biocell.2025.059432
    (This article belongs to the Special Issue: Cell Death and Inflammation in Signaling and Diseases)
    Abstract Z-DNA binding protein 1 (ZBP1) has emerged as a critical player in cancer biology, functioning as a cytosolic nucleic acid sensor that triggers PANoptosis, a form of programmed cell death that integrates pyroptosis, apoptosis, and necroptosis. Although ZBP1 was initially recognized for its role in antiviral defense, recent research has highlighted its importance in the tumor microenvironment (TME), where it is essential for suppressing tumor growth and proliferation. This review explores the multifaceted role of ZBP1 in various cancer types, emphasizing its ability to detect Z-nucleic acids and double-stranded RNAs, leading to the initiation of… More >

  • Open Access

    REVIEW

    The Role of Glutamate Receptors in Ischemic Stroke

    Long Qi, Chaoran Wu, Hao Sun, Hong Liao
    BIOCELL, Vol.49, No.2, pp. 167-180, 2025, DOI:10.32604/biocell.2025.059159
    (This article belongs to the Special Issue: Cell Death and Inflammation in Signaling and Diseases)
    Abstract Glutamate is an essential excitatory neurotransmitter in the brain, playing a vital role in regulating synaptic activity and maintaining the homeostasis of the cerebral environment but also serves as a central hub for neuronal injury and inflammatory responses. In various pathological conditions, such as ischemic stroke, glutamate is released and accumulates excessively in the brain, leading to heightened stimulation of neurons and excitotoxicity. This phenomenon positions glutamate as a primary inducing factor for neuronal damage following cerebral ischemia. Glutamate exerts its effects primarily through two types of receptors: ionotropic and metabotropic glutamate receptors, both of… More >

  • Open Access

    REVIEW

    Unraveling the molecular crossroads: T2DM and Parkinson’s disease interactions

    TINGTING LIU, XIANGRUI KONG, JIANSHE WEI
    BIOCELL, Vol.48, No.12, pp. 1735-1749, 2024, DOI:10.32604/biocell.2024.056272
    (This article belongs to the Special Issue: Cell Death and Inflammation in Signaling and Diseases)
    Abstract Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by persistent hyperglycemia. In recent times, an elevated risk of Parkinson’s disease (PD) development among individuals with T2DM has become evident. However, the molecular mechanisms that underpin the interplay between T2DM and the pathogenesis of PD remain to be elucidated. Nevertheless, recent epidemiological studies have underscored several shared molecular pathways that are crucial for normal cellular function and are also associated with the progression and etiology of both T2DM and PD. This review encapsulates some of the shared pathophysiological mechanisms, including genetic risk factors, More >

  • Open Access

    ARTICLE

    Tanshinone IIA inhibits NLRP3 activation and attenuates alveolar macrophage pyroptosis via the TREM2/β-catenin pathway

    MIN LIU, XIA LI, JUN LIU, YU LIU
    BIOCELL, Vol.48, No.10, pp. 1475-1487, 2024, DOI:10.32604/biocell.2024.053227
    (This article belongs to the Special Issue: Cell Death and Inflammation in Signaling and Diseases)
    Abstract Background: Alveolar macrophage pyroptosis exacerbates inflammatory lung diseases, and tanshinone IIA is known for its anti-inflammatory properties. Thus, understanding how tanshinone IIA affects alveolar macrophage pyroptosis is essential. Methods: NR8383 cells were exposed to lipopolysaccharide (LPS) and adenosine triphosphate (ATP). We assessed cell viability, pyroptosis, and the expression of triggering receptors expressed on myeloid cells 2 (TREM2), p-β-catenin, β-catenin, and pyroptosis-related factors. We also examined the interaction between tanshinone IIA and TREM2. Results: Co-stimulation with LPS and ATP significantly reduced NR8383 cell viability, increased pyroptosis, and upregulated pyroptosis-associated factors. Treatment with tanshinone IIA mitigated these effects.… More >

  • Open Access

    ARTICLE

    Lovastatin modulation of YAP/TAZ signaling on cardiomyocyte autophagy and mitochondrial damage in myocardial I/R injury

    KAITIAN ZHANG, MINGZHU LI, JIANPING ZHANG, JINFENG LI, KUNLANG LI, HUANQIAN LU, JINYAN LV
    BIOCELL, Vol.48, No.10, pp. 1489-1501, 2024, DOI:10.32604/biocell.2024.053930
    (This article belongs to the Special Issue: Cell Death and Inflammation in Signaling and Diseases)
    Abstract Objective: Studies have demonstrated that administering statins promptly following myocardial ischemia/reperfusion (MI/R) can confer cardioprotective benefits. This study investigates whether Lovastatin can modulate the Yes-associated protein/Transcriptional co-activator with PDZ-binding motif (YAP/TAZ) signaling pathway to mitigate cardiomyocyte injury caused by hypoxia/reoxygenation (H/R). Methods: The in vitro MI/R model was established by H/R in rat myocardial H9c2 cells, and the cells were pretreated with varying doses of Lovastatin before reoxygenation. The extent of cellular injury was evaluated by measuring the myocardial enzyme content and cell viability. The levels of oxidative stress and inflammatory factors were quantified by enzyme-linked… More >

    Graphic Abstract

    Lovastatin modulation of YAP/TAZ signaling on cardiomyocyte autophagy and mitochondrial damage in myocardial I/R injury

  • Open Access

    ARTICLE

    Single-cell transcriptomics reveals T-cell heterogeneity and immunomodulatory role of CD4+ T native cells in Candida albicans infection

    KERAN JIA, YANHAO ZHANG, MENGYU JIANG, MENGGE CUI, JIA WANG, JIAJIA ZHANG, HUIHAI ZHAO, MENGYAN LI, HUA WANG, QUANMING ZOU, HAO ZENG
    BIOCELL, Vol.48, No.9, pp. 1355-1368, 2024, DOI:10.32604/biocell.2024.051383
    (This article belongs to the Special Issue: Cell Death and Inflammation in Signaling and Diseases)
    Abstract Objective: Candida albicans is a common fungal pathogen that triggers complex host defense mechanisms, including coordinated innate and adaptive immune responses, to neutralize invading fungi effectively. Exploring the immune microenvironment has the potential to inform the development of therapeutic strategies for fungal infections. Methods: The study analyzed individual immune cell profiles in peripheral blood mononuclear cells from Candida albicans-infected mice and healthy control mice using single-cell transcriptomics, fluorescence quantitative PCR, and Western blotting. We investigated intergroup differences in the dynamics of immune cell subpopulation infiltration, pathway enrichment, and differentiation during Candida albicans infection. Results: Our findings indicate that infiltration… More >

  • Open Access

    ARTICLE

    UBE2T mediates the stemness properties of breast cancer cells through the mTOR signaling pathway

    JIAWEI YIN, YONGSHENG WANG, GUANGWEI WEI, MINGXIN WEN
    BIOCELL, Vol.48, No.6, pp. 959-970, 2024, DOI:10.32604/biocell.2024.049349
    (This article belongs to the Special Issue: Cell Death and Inflammation in Signaling and Diseases)
    Abstract Objectives: This study aimed to reveal the role and possible mechanism of the ubiquitin-conjugating enzyme 2T (UBE2T) in the biological activities of breast cancer stem cells (BCSCs). Methods: The specific protein and gene expression were quantified by Western blotting and quantitative real-time polymerase chain reaction, the proportion of BCSCs was examined by flow cytometry, and the self-renewal and proliferation of BCSCs were verified by serial sphere formation and soft agar. Results: Increasing expression of UBE2T was drastically found in breast cancer than that in adjacent tissues. Furthermore, UBE2T overexpression significantly increased the proportion of BCSCs in More >

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