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Biomedicines
Special Issues
Connective Tissue Disorders: Pathogenetic, Diagnostic and Therapeutic Perspectives
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Connective Tissue Disorders: Pathogenetic, Diagnostic and Therapeutic Perspectives

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 1300

Special Issue Editor

Prof. Dr. Katarzyna Winsz-Szczotka

E-Mail Website
Guest Editor
Laboratory Diagnostics, Department of Clinical Chemistry, Faculty of Pharmaceutical Sciences in Sosnowiec, Medical University of Silesia, Sosnowiec, Poland
Interests: connective tissue diseases; pathology of the extracellular matrix; growth factors; juvenile idiopathic arthritis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue on Connective Tissue Disorders (CTDs) aims to provide a comprehensive platform for sharing knowledge and experience on the latest advances in understanding the pathogenesis as well as diagnostic and therapeutic tools of CTDs.

CTDs are a heterogeneous group of clinical entities sharing a common feature, i.e., impairment of structural extracellular matrix components, in particular collagen or elastin, arising from autoimmune/autoinflammatory mechanisms. The risk-stratified patients with CTDs have a central role in predicting both organ involvement and disease progression. There is an ongoing effort to understand which factors are most important.

Researchers, clinicians and experts on these issues are encouraged to contribute their valuable insights to advance our knowledge regarding pathogenetic, diagnostic and therapeutic perspectives on these diseases. Articles on advances in autoimmunity and auto-inflammation as well as those that advance our knowledge on the loss and accumulation of extracellular matrix components are welcome for this Special Issue. We welcome your research and comments on these topics.

Prof. Dr. Katarzyna Winsz-Szczotka
Guest Editor

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. Biomedicines 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 2600 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

  • connective tissue disorders
  • pathophysiological mechanisms
  • inflammation
  • autoimmunity
  • extracellular matrix
  • fibrosis
  • biomarkers
  • treatment
  • therapeutic targets

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Published Papers (2 papers)

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Research

16 pages, 2695 KiB  
Article
Inflammatory Biomarkers and Lipid Parameters May Predict an Increased Risk for Atrial Arrhythmias in Patients with Systemic Sclerosis
by Veronika Sebestyén, Dóra Ujvárosy, Balázs Ratku, Hajnalka Lőrincz, Sára Csiha, Dóra Tari, Gyöngyike Majai, Sándor Somodi, Gabriella Szűcs, Mariann Harangi and Zoltán Szabó
Biomedicines 2025, 13(1), 220; https://doi.org/10.3390/biomedicines13010220 - 16 Jan 2025
Viewed by 468
Abstract
Background/Objectives: Autoimmune inflammation enhances the electrical instability of the atrial myocardium in patients with systemic sclerosis (SSc); thus, atrial arrhythmia risk is increased, which might be predicted by evaluating the P wave interval and dispersion of a 12-lead surface electrocardiogram (ECG). Methods: We [...] Read more.
Background/Objectives: Autoimmune inflammation enhances the electrical instability of the atrial myocardium in patients with systemic sclerosis (SSc); thus, atrial arrhythmia risk is increased, which might be predicted by evaluating the P wave interval and dispersion of a 12-lead surface electrocardiogram (ECG). Methods: We examined 26 SSc patients and 36 healthy controls and measured the P wave interval and P wave dispersion of the 12-lead surface ECG in each patient. Furthermore, echocardiography and 24-h Holter ECG were performed and levels of inflammatory laboratory parameters, including serum progranulin (PGRN), sVCAM-1, sICAM-1, leptin and C-reactive protein (CRP), were determined. Lipid parameters, such as Apo A-I, LDL-cholesterol (LDL-C), oxidized LDL (oxLDL) and the LDL and HDL subfractions were also evaluated. Results: The P wave interval showed a significant positive correlation with the levels of Apo A-I, LDL-C, CRP, sVCAM-1, sICAM-1 and leptin. The oxLDL level correlated positively with P wave dispersion. Of note, significant positive correlation was also found between the large HDL percentage and the P wave interval. Conclusions: Our results suggest that PGRN, sVCAM-1, sICAM-1, leptin, CRP, LDL-C and oxLDL, along with LDL and HDL subfractions, might have a role in atrial arrhythmogenesis in patients with SSc. Full article
(This article belongs to the Special Issue Connective Tissue Disorders: Pathogenetic, Diagnostic and Therapeutic Perspectives)
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12 pages, 1895 KiB  
Article
Craniofacial Effects of Zoledronic Acid on the Osteogenesis Imperfecta Mouse (−/−) Model of Severe Osteogenesis Imperfecta
by Gaspard Jeannerod, Antoine Chretien, Grégoire André, Guillaume Mabilleau and Catherine Behets
Biomedicines 2024, 12(12), 2692; https://doi.org/10.3390/biomedicines12122692 - 25 Nov 2024
Viewed by 581
Abstract
Background: Osteogenesis imperfecta (OI) is a rare genetic disorder affecting mainly type I collagen, which leads to bone fragility and deformities. OI patients also present craniofacial abnormalities such as macrocephaly and malocclusion. Recently, craniofacial dysmorphism was highlighted in the osteogenesis imperfecta mouse (oim), [...] Read more.
Background: Osteogenesis imperfecta (OI) is a rare genetic disorder affecting mainly type I collagen, which leads to bone fragility and deformities. OI patients also present craniofacial abnormalities such as macrocephaly and malocclusion. Recently, craniofacial dysmorphism was highlighted in the osteogenesis imperfecta mouse (oim), a validated model of the most severe form of OI. This study explores the impact of zoledronic acid (ZA), commonly administered to OI patients to increase bone mass and mechanical strength, on oim craniofacial structure. Methods: Fifteen oim received a single intravenous ZA injection (100 µg/kg) at 5 weeks (ZA group), while fifteen remained untreated (control). Before euthanasia at 14 weeks, in vivo computed tomography provided craniometric data. Post-euthanasia, heads underwent peripheral Quantitative Computed Tomography (pQCT); coronal decalcified sections through temporomandibular joints were analyzed (n = 6/mouse) after Masson’s trichrome staining (3 sections) or under polarized light to study collagen birefringence (3 sections). Results: In vivo craniometry highlighted the positive effect on vertical growth in ZA oim models as compared to untreated ones, with significant increases in mandibular length and incisor height and without any change in transversal dimensions. The pQCT scans showed the significantly higher total mineral density and cortical mineral density of the mandibular ramus in the ZA than the untreated group. Via microscopic analysis, the cranial vault was thicker and the collagen birefringence was higher in the ZA group than in the untreated group, but differences were not significant. Conclusion: To conclude, ZA had some beneficial effects on craniofacial vertical height and ramus density and, to a lower extent, on vault thickness, while transversal dimensions did not seem to be influenced by ZA intake. These data emphasize the need to consider the whole skeleton when treating OI patients. Full article
(This article belongs to the Special Issue Connective Tissue Disorders: Pathogenetic, Diagnostic and Therapeutic Perspectives)
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