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25th Anniversary of IJMS: Updates and Advances in Molecular Pathology, Diagnostics, and Therapeutics

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 January 2026 | Viewed by 826

Special Issue Editors

Dr. Francesca Oliviero

E-Mail Website
Guest Editor
Rheumatology Unit, Department of Medicine DIMED, University of Padova, 35128 Padova, Italy
Interests: pathogenetic mechanisms in crystal-induced inflammation; the role of calcium crystals in osteoarthritis; biomarkers in psoriatic arthritis; synovial fluid analysis; the influence of bioactive compounds in inflammation and crystal-induced arthritis; diet in rheumatic diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Anna Lisa Giuliani

E-Mail Website
Guest Editor
Department of Medical Sciences, University of Ferrara, Via Borsari 46, 44121 Ferrara, Italy
Interests: cancer research; cell culture; immunology; molecular biology; cancer biology; signaling pathways; cell biology; antibodies; inflammation; flow cytometry
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

I am honored to be the Guest Editor of this Special Issue of International Journal of Molecular Sciences (IJMS), titled "25th Anniversary of IJMS: Updates and Advances in Molecular Pathology, Diagnostics, and Therapeutics". This commemorative issue will mark the 25th anniversary of IJMS by showcasing the latest updates and advances in the field of molecular pathology, diagnostics, and therapeutics.

We invite contributions that explore molecular mechanisms underlying diseases, novel diagnostic approaches, and cutting-edge therapeutic strategies. This Special Issue will provide a comprehensive overview of the current state of research, highlighting groundbreaking discoveries and emerging trends in areas such as the following:

- Molecular and cellular mechanisms underlying diseases and injury;

- Immunopathology and immune-mediated disorders;

- Matrix pathobiology and tissue alterations;

- Molecular diagnostics and targeted therapies;

- Cell injury, repair, aging, and apoptosis;

- Stem cell and gene therapies;

- Novel mechanisms of carcinogenesis;

- Applications of molecular pathology in forensics and tissue identification.

We welcome original research articles, reviews, and perspectives from experts in the field, fostering interdisciplinary collaborations and advancing our understanding of molecular pathology, diagnostics, and therapeutics.

Dr. Francesca Oliviero
Dr. Anna Lisa Giuliani
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • molecular mechanisms of diseases
  • diagnostic approaches
  • therapeutic strategies

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Published Papers (3 papers)

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Research

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21 pages, 2258 KB  
Article
Neurotransmitter Genes in the Nucleus Accumbens That Are Involved in the Development of a Behavioral Pathology After Positive Fighting Experiences and Their Deprivation: A Conceptual Paradigm for Data Analysis
by Natalia N. Kudryavtseva, Dmitry A. Smagin, Olga E. Redina, Irina L. Kovalenko, Anna G. Galyamina and Vladimir N. Babenko
Int. J. Mol. Sci. 2025, 26(17), 8580; https://doi.org/10.3390/ijms26178580 - 3 Sep 2025
Abstract
It has been shown previously that repeated positive fighting experience in daily agonistic interactions is accompanied by the development of psychosis-like behavior, with signs of an addiction-like state associated with changes in the expression of genes encoding the proteins involved in the main [...] Read more.
It has been shown previously that repeated positive fighting experience in daily agonistic interactions is accompanied by the development of psychosis-like behavior, with signs of an addiction-like state associated with changes in the expression of genes encoding the proteins involved in the main neurotransmitter events in some brain regions of aggressive male mice. Fighting deprivation (a no-fight period of 2 weeks) causes a significant increase in their aggressiveness. This paper is aimed at studying—after a period of fighting deprivation—the involvement of genes (associated with neurotransmitter systems within the nucleus accumbens) in the above phenomena. The nucleus accumbens is known to participate in reward-related mechanisms of aggression. We found the following differentially expressed genes (DEGs), whose expression significantly differed from that in controls and/or mice with positive fighting experience in daily agonistic interactions followed by fighting deprivation: catecholaminergic genes Th, Drd1, Drd2, Adra2c, Ppp1r1b, and Maoa; serotonergic genes Maoa, Htr1a, Htr1f, and Htr3a; opioidergic genes Oprk1, Pdyn, and Penk; and glutamatergic genes Grid1, Grik4, Grik5, Grin3a, Grm2, Grm5, Grm7, and Gad1. The expression of DEGs encoding proteins of the GABAergic system in experienced aggressive male mice mostly returned to control levels after fighting deprivation, except for Gabra5. In light of the conceptual paradigm for analyzing data that was chosen in our study, the aforementioned DEGs associated with the behavioral pathology can be considered responsible for consequences of aggression followed by fighting deprivation, including mechanisms of an aggression relapse. Full article
(This article belongs to the Special Issue 25th Anniversary of IJMS: Updates and Advances in Molecular Pathology, Diagnostics, and Therapeutics)
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13 pages, 802 KB  
Article
Salivary Protein Profile in Patients with Recurrent Aphthous Stomatitis: A Pilot Proteomic Study
by Francesco Franco, Nima Namarvari, Alessio Gambino, Federica Romano, Barbara Pergolizzi, Jianjian Zhang, Giuliana Abbadessa, Barbara Mognetti, Adriano Ceccarelli, Paolo Giacomo Arduino and Giovanni Nicolao Berta
Int. J. Mol. Sci. 2025, 26(16), 7878; https://doi.org/10.3390/ijms26167878 - 15 Aug 2025
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Abstract
Recurrent aphthous stomatitis (RAS) is the most common ulcerative disorder of the oral cavity, although its etiology is still unknown. The present study aimed to identify the proteomic profile associated with the RAS inflammatory process, thereby enhancing our understanding of its etiopathogenesis. We [...] Read more.
Recurrent aphthous stomatitis (RAS) is the most common ulcerative disorder of the oral cavity, although its etiology is still unknown. The present study aimed to identify the proteomic profile associated with the RAS inflammatory process, thereby enhancing our understanding of its etiopathogenesis. We compared salivary protein profiles of RAS patients during an active episode of oral ulceration (30 patients, mean age 36.9) to those from healthy donors without a history of RAS (30 healthy subjects, mean age 37.9). Using 2D-electrophoresis and mass spectrometry (MALDI-TOF) analysis, we identified 17 proteins that were differentially expressed in the two groups. Notably, Cystatin SN (CST1) appeared to be significantly downregulated in RAS patients. These findings were validated by Western blot analysis: CST1 was detected in only 3 of the 30 RAS cases, while it was strongly expressed in all the healthy subjects. Although preliminary, our results suggest a potential role for CST1 in the etiopathogenesis of RAS. Interestingly, the relative absence of CST1 in RAS patients seems to align with some clinical and molecular features of this disease. Full article
(This article belongs to the Special Issue 25th Anniversary of IJMS: Updates and Advances in Molecular Pathology, Diagnostics, and Therapeutics)
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Review

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21 pages, 820 KB  
Review
Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Pathophysiology, Clinical Patterns, and Therapeutic Challenges of Intractable and Severe Forms
by Tatsuro Misu
Int. J. Mol. Sci. 2025, 26(17), 8538; https://doi.org/10.3390/ijms26178538 - 2 Sep 2025
Viewed by 210
Abstract
Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is characterized by the predominance of optic neuritis, myelitis, acute disseminated encephalomyelitis (ADEM), and cortical encephalitis, and can be diagnosed by the presence of pathogenic immunoglobulin G (IgG) antibodies targeting the extracellular domain of MOG in [...] Read more.
Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is characterized by the predominance of optic neuritis, myelitis, acute disseminated encephalomyelitis (ADEM), and cortical encephalitis, and can be diagnosed by the presence of pathogenic immunoglobulin G (IgG) antibodies targeting the extracellular domain of MOG in the serum and cerebrospinal fluid (CSF). Initially considered a variant of multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD), it is now widely recognized as a separate entity, supported by converging evidence from serological, pathological, and clinical studies. Patients with MOGAD often exhibit better recovery from acute attacks; however, their clinical and pathological features vary based on the immunological role of MOG-IgG via antibody- or complement-mediated perivenous demyelinating pathology, in addition to MOG-specific cellular immunity, resulting in heterogeneous demyelinated lesions from vanishing benign forms to tissue necrosis, even though MOGAD is not a mild disease. The key is the immunological mechanism of devastating lesion coalescence and long-term degenerating mechanisms, which may still accrue, particularly in the relapsing, progressing, and aggressive clinical course of encephalomyelitis. The warning features of the severe clinical forms are: (1) fulminant acute multifocal lesions or multiphasic ADEM transitioning to diffuse (Schilder-type) or tumefactive lesions; (2) cortical or subcortical lesions related to brain atrophy and/or refractory epilepsy (Rasmussen-type); (3) longitudinally extended spinal cord lesions severely affected with residual symptoms. In addition, it is cautious for patients refractory to acute stage early 1st treatment including intravenous methylprednisolone treatment and apheresis with residual symptoms and relapse activity with immunoglobulin and other 2nd line treatments including B cell depletion therapy. Persistent MOG-IgG high titration, intrathecal production of MOG-IgG, and suggestive markers of higher disease activity, such as cerebrospinal fluid interleukin-6 and complement C5b-9, could be identified as promising markers of higher disease activity, worsening of disability, and poor prognosis, and used to identify signs of escalating treatment strategies. It is promising of currently ongoing investigational antibodies against anti-interleukin-6 receptor and the neonatal Fc receptor. Moreover, due to possible refractory issues such as the intrathecal production of autoantibody and the involvement of complement in the worsening of the lesion, further developments of other mechanisms of action such as chimeric antigen receptor T-cell (CAR-T) and anti-complement therapies are warranted in the future. Full article
(This article belongs to the Special Issue 25th Anniversary of IJMS: Updates and Advances in Molecular Pathology, Diagnostics, and Therapeutics)
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