Submit to Special Issue Submit Abstract to Special Issue Review for CIMB Propose a Special Issue

Journal Menu

Journal Browser

Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions, 2nd Edition

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Keywords
Benefits of Publishing in a Special Issue
Published Papers

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 7133

Share This Special Issue

Special Issue Editors

Prof. Dr. Hector A. Cabrera-Fuentes

E-Mail Website
Guest Editor

1. UNAM-UABJO Research Center, Universidad Autónoma Benito Juárez de Oaxaca, Oaxaca 68120, Mexico
2. Division of Postgraduate Studies and Research, Tijuana Institute of Technology, National Technological of Mexico (TecNM), Tijuana 22414, Mexico
Interests: basic science and clinical research in organ protection against acute ischaemia/reperfudion injury with a special focus on cardiac protection and acute inflammation and remodeling; basic science and translational research in atherosclerosis and chronic inflammation processes
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Klaus T. Preissner

E-Mail Website
Guest Editor

Department of Cardiology, Kerckhoff-Heart Research Institute, Faculty of Medicine, Justus-Liebig-University, 35392 Giessen, Germany
Interests: innate immune processes in host-pathogen interactions; inflammation; wound healing; thrombosis; cardiovascular diseases; lung disease
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Elisabeth Deindl

E-Mail Website
Guest Editor

1. Walter-Brendel-Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-Universität, 81377 Munich, Germany
2. Biomedical Center, Institute of Cardiovascular Physiology and Pathophysiology, Ludwig-Maximilians-Universität München, Planegg-Martinsried, 82152 Munich, Germany
3. Institute of Surgical Research, Walter Brendel Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany
Interests: cardiovascular research; immunology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammatory diseases, ranging from autoimmune disorders to chronic inflammatory conditions, pose significant challenges to global health. The complexity of inflammation involves intricate molecular pathways, including immune system dysregulation, cytokine signaling and oxidative stress, which vary among individuals and disease states. Advances in molecular biology and precision medicine are unlocking new insights into these mechanisms, offering the potential for highly targeted and effective therapies. This Special Issue aims to delve into the molecular mechanisms that drive inflammatory diseases, with a focus on identifying novel therapeutic targets and pathways. By exploring innovative therapeutic approaches—such as biologics, small molecules, gene therapies and personalized treatment regimens—this Special Issue will shed light on the future of inflammation treatment through precision medicine. We invite submissions that provide groundbreaking research, clinical studies and reviews on molecular drivers of inflammation, disease biomarkers and personalized therapeutic strategies that hold the potential to transform patient outcomes in inflammatory diseases.

You can read the publications in the first volume of this Special Issue here:

https://www.mdpi.com/journal/cimb/special_issues/64WAEHH553

Prof. Dr. Hector A. Cabrera-Fuentes
Prof. Dr. Klaus Preissner
Prof. Dr. Elisabeth Deindl
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. Current Issues in Molecular Biology is an international peer-reviewed open access monthly 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 2200 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

inflammatory diseases
autoimmune disorders
cytokine signaling
oxidative stress
therapies

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 (9 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review, Other

15 pages, 3464 KB

Open AccessArticle

Inflammation-Linked Muscle Atrophy in Limb Girdle Muscular Dystrophy R1 (LGMDR1): Insights into Disease Mechanisms

by Sukanya Banerjee, Bishan Dass Radotra, Manni Luthra-Guptasarma and Manoj K. Goyal

Curr. Issues Mol. Biol. 2026, 48(4), 361; https://doi.org/10.3390/cimb48040361 - 30 Mar 2026

Viewed by 441

Abstract

Background: Muscle atrophy is a major feature of Limb Girdle Muscular Dystrophy R1 (LGMDR1) patients, but its underlying molecular mechanisms have not been fully explored. While the ubiquitin–proteasome system (UPS) is known to be involved in muscle protein degradation, inflammation commonly observed in LGMDR1 patients may further activate the UPS. This study aimed to explore the role of inflammation in the muscle atrophy of LGMDR1 patients. Methods: Muscle biopsies from six confirmed LGMDR1 patients (with CAPN3 variants and reduced calpain-3 protein expression) were analyzed for atrophy-related markers, MuRF1 and Atrogin-1, using qRT-PCR and Western blotting. The expression of cytokines, TNF-α, IL-1β, and IL-6 was analyzed by qRT-PCR from muscle biopsies and by ELISA from serum samples. The NFκB, FOXO1, and FOXO3 gene expression was analyzed using qRT-PCR and Western blotting from muscle biopsies. Results: Elevated TNF-α levels were associated with increased UPS activity, reflected by upregulated NFκB, FOXO1, MuRF1, and Atrogin-1 expression in LGMDR1. Conclusion: Our findings indicate that increased TNF-α expression is associated with muscle wasting in LGMDR1 patients by targeting UPS pathway mediators that activate ubiquitin ligases—MuRF1 and Atrogin-1. These findings suggest that targeting TNF-α signaling and its downstream factors may help develop therapeutic interventions to prevent muscle atrophy in LGMDR1 patients. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions, 2nd Edition)

► Show Figures

Figure 1

10 pages, 223 KB

Open AccessArticle

Personalized Immunotherapy in Osteoarthritis: A Clinical Trial of Autologous Dendritic Cell Immunotherapy in Knee Osteo-Arthritis

by Kurniawan Silalahi, Bhimo Aji Hernowo, Jonny Jonny, Lintang Sagoro, Chrismis Novalinda Ginting and Terawan Agus Putranto

Curr. Issues Mol. Biol. 2026, 48(3), 330; https://doi.org/10.3390/cimb48030330 - 20 Mar 2026

Viewed by 492

Abstract

Background/Objectives: Osteoarthritis (OA) is a chronic inflammatory disease with limited disease-modifying therapies. This study explored a novel immunomodulatory approach using autologous, antigen-pulsed semi-mature dendritic cells (DCs) to modulate the inflammatory milieu in knee OA patients. Methods: In this open-label, quasi-experimental study, 29 subjects received a single subcutaneous injection of autologous DCs. Outcomes assessed at baseline and 4 weeks included the WOMAC index for symptoms and serum levels of IL-6 and TNF-α. Responses were analyzed in the overall cohort and by BMI subgroups. Results: The overall cohort showed a non-significant trend in WOMAC improvement (p = 0.080) and no change in IL-6 (p = 0.785) or TNF-α (p = 0.330). Subgroup analysis revealed differential patterns of response: WOMAC scores improved significantly only in normal-weight patients (p = 0.030), while serum TNF-α decreased significantly only in overweight patients (p = 0.025). IL-6 levels were unchanged across all groups. Conclusions: Autologous antigen-pulsed DC administration was associated with differential responses across BMI subgroups. Symptomatic benefit was observed in normal-weight individuals, while a reduction in systemic TNF-α occurred in overweight patients. These findings suggest that the host metabolic state may modulate the response to DC-based immunotherapy, and therefore warrant validation in a randomized, placebo-controlled trial. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions, 2nd Edition)

17 pages, 5967 KB

Open AccessArticle

Treatment with Sildenafil Promotes Angiogenesis and Modulates Immune Response in Ischemic Muscle Tissue

by Amelie Kuhs, Lisa Bobrowski, Katharina Elbs, Matthias Kübler, Philipp Götz, Christoph Arnholdt, Manuel Lasch and Elisabeth Deindl

Curr. Issues Mol. Biol. 2026, 48(3), 283; https://doi.org/10.3390/cimb48030283 - 6 Mar 2026

Viewed by 616

Abstract

Sildenafil, a selective phosphodiesterase-5 (PDE5) inhibitor, supports vascular remodeling, but its effects on angiogenesis and regeneration of ischemic muscle tissue are not fully understood. We investigated the function of sildenafil by employing a murine hindlimb model of ischemia, in which ischemia and angiogenesis is induced by femoral artery ligation (FAL) in the lower leg of mice. Then, 7 days after FAL or sham operation, gastrocnemius muscles of sildenafil-treated and control mice were isolated and processed for histological and immunofluorescence analyses. Sildenafil treatment led to reduced apoptotic areas within the ischemic tissue (ascertained via TUNEL assay) and increased angiogenesis, evidenced by a higher capillary-to-muscle fiber ratio and an augmented number of proliferating capillary cells (CD31⁺/CD45⁻/BrdU⁺), compared to controls. We observed a decrease in the total count of leukocytes (CD45⁺) in sildenafil-treated mice. Regarding macrophage infiltration, we found a reduced total number of macrophages (CD68⁺), along with a shift in macrophage polarization toward the pro-angiogenic and anti-inflammatory M2-like phenotype (CD68⁺/MRC1⁺). In summary, we show that sildenafil treatment contributes to angiogenesis and the regeneration of ischemic muscle tissue, most likely by attenuating inflammatory responses and influencing macrophage polarization in direction to regenerative M2-like polarized macrophages. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions, 2nd Edition)

► Show Figures

Figure 1

18 pages, 20606 KB

Open AccessArticle

IL-37 Ameliorates Chronic Endometritis by Attenuating Epithelial—Mesenchymal Transition and Promoting M2 Macrophage Polarization

by Zihan Wang, Jiaxi Tan, Rui Zhang, Xuanyu Liu, Huihui Zhang and Xia Zhang

Curr. Issues Mol. Biol. 2026, 48(2), 227; https://doi.org/10.3390/cimb48020227 - 20 Feb 2026

Cited by 1 | Viewed by 460

Abstract

Interleukin-37 (IL-37) is an anti-inflammatory cytokine with an undefined role in chronic endometritis (CE). This study aims to explore its therapeutic mechanism in CE, focusing on epithelial-mesenchymal transition (EMT) and macrophage polarization. A CE model was induced in Sprague-Dawley rats using lipopolysaccharide (LPS), followed by intervention with TAT-fused recombinant IL-37. Histological damage and fibrosis were evaluated through H&E and Masson staining. Immunofluorescence staining was performed to assess the expression of IL-37 and EMT markers (E-cadherin and vimentin) and macrophage phenotypes (M1: CD86⁺; M2: CD206⁺). In vitro, transwell, qPCR, Western blot, and flow cytometry analyses were performed to determine the effects of IL-37 on EMT and macrophage polarization. The activity of the STAT6 and Smad3 pathways was evaluated using Western blotting, dual-luciferase assays, and immunofluorescence staining. The results revealed that IL-37 accumulated in the injured uterus, alleviating inflammation, tissue damage, and collagen deposition. IL-37 reduced epithelial migration and reversed abnormal EMT by upregulating E-cadherin expression and downregulating vimentin expression. It also suppressed M1 macrophage infiltration and promoted M2 polarization. Mechanistically, IL-37 coactivated the STAT6 and Smad3 pathways, thereby increasing their phosphorylation and nuclear translocation and elevating ARG1 expression. In conclusion, IL-37 mitigates CE by suppressing EMT and promoting M2 macrophage polarization via coordinated STAT6/Smad3 activation, highlighting its therapeutic potential for CE. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions, 2nd Edition)

► Show Figures

Figure 1

19 pages, 3480 KB

Open AccessArticle

Therapeutic Insights and Immune Pathway Connections Revealed by Core Symptom Gene Network Analysis in Ankylosing Spondylitis

by La Yoon Choi, Mi Hye Kim and Dae Yong Kim

Curr. Issues Mol. Biol. 2026, 48(2), 199; https://doi.org/10.3390/cimb48020199 - 11 Feb 2026

Viewed by 638

Abstract

Ankylosing spondylitis (AS) exhibits marked clinical heterogeneity that is poorly captured by conventional disease-centric analyses, hindering the development of personalized therapies. We propose a symptom-centered network pharmacology framework that directly links individual clinical symptoms to their underlying molecular mechanisms and therapeutic targets. AS- and symptom-associated genes were collected from GeneCards and prioritized using centrality analysis within protein–protein interaction networks. Symptom relevance was validated using patient-derived transcriptomic datasets. Network proximity between symptom modules and FDA-approved drug targets was assessed. A refined gene set, integrating TNF-associated neighbors and highly central nodes, was subjected to pathway enrichment analysis. Disease-centric analysis yielded a restricted 18-gene core enriched mainly in broad immune pathways. In contrast, the symptom-centered network identified 145 genes associated with specific symptoms such as inflammatory back pain and morning stiffness. Key genes, including PTEN, TLR4, JAK2, NRAS, and NR3C1, were significantly upregulated in AS patients. TNF showed local connectivity but limited global proximity, while IL17A- and JAK inhibitor-related targets were absent. A refined 24-gene module revealed enrichment in interleukin- and cytokine-mediated signaling pathways. Symptom-centered network analysis more effectively captures molecular heterogeneity in AS, providing a robust framework for symptom-specific target discovery and personalized therapeutic strategies. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions, 2nd Edition)

► Show Figures

Figure 1

32 pages, 9773 KB

Open AccessArticle

From Gas Chromatography–Mass Spectrometry (GC–MS) to Network Pharmacology: System-Level Insights into the Multi-Target Biological Potential of Flaveria trinervia (Spreng.) C. Mohr

by Christopher Torres Flores, Eduardo Pérez-Campos, Laura Pérez-Campos Mayoral, Luis Ángel Laguna-Barrios, Karen Beatriz Méndez-Rodríguez, Francisco Javier Pérez-Vázquez, Eduardo Pérez Campos-Mayoral, Carlos Mauricio Lastre-Domínguez, Efrén Emmanuel Jarquín González, Margarito Martínez Cruz, María del Socorro Pina Canseco, Zoila Mora Guzmán, Karol Celeste López Montesinos, Hector A. Cabrera-Fuentes and María Teresa Hernández-Huerta

Curr. Issues Mol. Biol. 2026, 48(2), 160; https://doi.org/10.3390/cimb48020160 - 1 Feb 2026

Viewed by 1039

Abstract

Flaveria trinervia (Spreng) C. Mohr is a plant traditionally used in Mexican medicine. In this study, gas chromatography–mass spectrometry (GC–MS) combined with network pharmacology was employed to characterize volatile and semi-volatile metabolites from F. trinervia leaves and to explore their potential system-level mechanisms of action in inflammatory and tumor-related disorders. A dual extraction strategy (hexane/dichloromethane and acetone/chloroform) was applied, followed by GC–MS-based compound identification. Putative molecular targets were predicted using established pharmacological databases, and protein–protein interaction networks were constructed to identify topological features and enriched biological pathways. A total of 11 bioactive compounds were tentatively identified with an identity level of ≥80%, with seven shared between both extracts, including phytol, germacrene D, caryophyllene oxide, pinene isomers, squalene, and 2,2′:5′,2″-terthiophene, metabolites previously reported to exhibit antioxidant, anti-inflammatory, and cytotoxic activities. Network topology analysis identified ESR1, RXRA/B/G, NCOA2, and CYP19A1 as central nodes, reflecting convergence on signaling axes involved in apoptosis, cell proliferation, immune modulation, and transcriptional regulation pathways. Functional enrichment analysis revealed significant associations with KEGG pathways related to immune modulation, neuroendocrine regulation, and cancer-associated pathways. Collectively, these findings suggest a multitarget biological and multipathway pharmacological profile for F. trinervia, consistent with previously reported biological activities. The concordance between in silico predictions and existing experimental evidence strengthens the pharmacological relevance of the identified metabolites and supports their prioritization for further experimental validation, including mechanistic and pharmacokinetic studies, in metabolic, immune, neurological, and cancer-related contexts. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions, 2nd Edition)

► Show Figures

Graphical abstract

14 pages, 412 KB

Open AccessArticle

Host Immunogenetic Profile Modulates Susceptibility to Apical Periodontitis in a Colombian Population

by Ingrid Giraldo-Quiceno, Natalia Andrea Torres-Calvo, Andrés Felipe Ayala-Jaramillo, Christina Garcés, Sandra Catalina Garzón-Castaño, Beatriz Giraldo-Ospina, Nora Elena Valencia-Marroquín, Carlos Manuel Beltrán-Díaz, Iván Alberto Lopera-Castrillón and Carlos Andrés Naranjo-Galvis

Curr. Issues Mol. Biol. 2026, 48(1), 107; https://doi.org/10.3390/cimb48010107 - 20 Jan 2026

Viewed by 505

Abstract

Apical periodontitis (AP) is a chronic immunoinflammatory disease influenced by complex interactions between microbial factors and host immune response. Although genetic susceptibility has been implicated in AP, evidence is limited, particularly in admixed populations. This exploratory study aimed to assess whether functional polymorphisms in MMP1 (rs1799750), IL10 (rs1800872), and IL17A (rs7747909) are associated with susceptibility to radiographically defined AP in a Colombian population. A case–control design was employed, including individuals with radiographic evidence of AP and controls without periapical lesions. Genotyping was performed using TaqMan^® assay. The association between single-nucleotide polymorphisms and AP was evaluated using a dominant inheritance model. Effect sizes were estimated as odds ratios (ORs) with 95% confidence intervals (CIs), and p-values were adjusted using the Benjamini–Hochberg false discovery rate (FDR) procedure. The MMP1 rs1799750 polymorphism was associated with increased susceptibility to AP (OR = 3.47, 95% CI = 1.40–8.58; FDR = 0.013). Similarly, the IL10 rs1800872 variant was significantly associated with AP risk (OR = 3.00, 95% CI = 1.52–5.91; FDR = 0.007). The strongest association was observed for IL17A rs7747909 (OR = 8.95, 95% CI = 3.61–22.15; FDR < 0.001). This exploratory candidate-gene study provides preliminary evidence suggesting that genetic variations in MMP1, IL10, and IL17A may contribute to susceptibility to AP in the Colombian population. Given the exploratory design, modest sample size, and absence of ancestry adjustment or functional validation, these findings should be interpreted cautiously and confirmed in larger ancestry-informed cohorts integrating host genetic and microbial data. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions, 2nd Edition)

► Show Figures

Figure 1

Review

Jump to: Research, Other

19 pages, 1138 KB

Open AccessReview

Interleukin Signatures as Prognostic Biomarkers in Ulcerative Colitis: From Immune Pathways to Clinical Prediction

by Nikolaos Martinos, Andreas C. Lazaris, Christos Kroupis, Georgios Kranidiotis and Georgia-Eleni Thomopoulou

Curr. Issues Mol. Biol. 2026, 48(2), 140; https://doi.org/10.3390/cimb48020140 - 27 Jan 2026

Cited by 2 | Viewed by 2202

Abstract

Ulcerative colitis (UC) is a chronic immune-mediated inflammatory disease characterized by substantial heterogeneity in histologic activity, which is frequently uncoupled from clinical symptoms and endoscopic findings. Persistent microscopic inflammation is increasingly recognized as a critical determinant of relapse, therapeutic failure, and long-term disease outcomes, underscoring the need for molecular frameworks that align directly with tissue-level immune dysregulation. Interleukins (ILs) represent central regulators of mucosal immunity in UC, integrating innate and adaptive immune responses that govern epithelial injury and resolution. In this narrative review, we synthesize mechanistic, translational, genetic, and clinical evidence examining IL networks associated with histologic disease activity and persistence. Particular emphasis is placed on IL-23-driven inflammatory pathways, which consistently align with histologic severity, sustained microscopic inflammation, and resistance to immune resolution. In contrast, preserved IL-10-mediated regulatory signaling characterizes histologic remission and effective mucosal healing, whereas its insufficiency permits ongoing tissue-level inflammation. Downstream effector ILs, including IL-6, IL-1β, IL-8, and IL-17A, are discussed as mediators translating upstream immune imbalance into neutrophil recruitment and epithelial injury. Throughout this review, the term “prognostic” is used to denote alignment with histologic disease behavior rather than validated prediction of clinical outcomes. Collectively, the evidence supports the concept that coordinated IL patterns reflect distinct immunopathologic states underlying microscopic inflammation in UC, providing a biologically coherent framework for interpreting histologic activity and disease persistence beyond symptom-based assessment. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions, 2nd Edition)

► Show Figures

Graphical abstract

Other

Jump to: Research, Review

16 pages, 5015 KB

Open AccessPerspective

Serglycin Across the Disease Spectrum: A Multifunctional Proteoglycan in Inflammation and Cancer

by Eleftherios N. Athanasopoulos, Vassiliki T. Labropoulou and Achilleas D. Theocharis

Curr. Issues Mol. Biol. 2026, 48(5), 454; https://doi.org/10.3390/cimb48050454 - 28 Apr 2026

Viewed by 96

Abstract

The inflammatory response possesses a central role in human pathophysiology, regulating the tissue microenvironment and cell signaling. Inflammation occurs either as a symptom of homeostasis disturbance or as a driver for determining cell fate. In this context, cells recruit secreted cytokines, chemokines and intracellular mediators, in cooperation with their surrounding cellular components, to integrate inflammatory stimuli. The extracellular matrix (ECM) acts as a scaffold for shaping tissue structure and simultaneously undergoes continuous remodeling to provide a dynamic network for intercellular communication. Serglycin (SRGN) is the only known intracellular and extracellular proteoglycan, implicated in the formation of secretory vesicles and ECM reorganization. The regulatory roles of SRGN in the bioavailability of secreted factors, as well as SRGN pleiotropic interactions within the ECM, as well as with cell surface receptors, have emerged to beessential for inflammatory diseases and tumor progression. Its overexpression and excessive secretion, alongside its contribution to cell signaling, highlight the potential diagnostic and therapeutic aspects of SRGN in human diseases. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions, 2nd Edition)

► Show Figures

Journal Menu

Journal Browser

Molecular Mechanisms and Innovative Therapeutic Approaches in Inflammatory Diseases, Pioneering Precision Medicine Solutions, 2nd Edition

Share This Special Issue

Special Issue Editors

Special Issue Information

Keywords

Benefits of Publishing in a Special Issue

Published Papers (9 papers)

Research

Review

Other

Further Information

Guidelines

MDPI Initiatives

Follow MDPI