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Autoimmune Diseases and Cardiovascular System: Physiopathology, Epidemiology, Clinical Characteristics and...
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Autoimmune Diseases and Cardiovascular System: Physiopathology, Epidemiology, Clinical Characteristics and Therapeutic Strategies

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: 28 February 2025 | Viewed by 5611

Special Issue Editor

Prof. Dr. Gian Luca Erre

E-Mail Website
Guest Editor
Dipartimento di Medicina, Chirurgia e Farmacia, University of Sassari, 07100 Sassari, Italy
Interests: autoimmune disorders; rheumatic diseases; clinical rheumatology; rheumatoid arthritis; autoimmunity; atherosclerosis; endothelial dysfunction; cardiovascular disease; arterial stiffness; atrial myopathy

Special Issue Information

Dear Colleagues,

The impact of chronic autoimmune conditions on the development of cardiovascular disease is due to a broad range of conditions, including a chronic inflammatory burden, oxidative stress, the loss of tolerance, and the adverse effects of immunosuppressive and anti-inflammatory drugs. Patients with autoimmune diseases, including rheumatoid arthritis, lupus, psoriasis, multiple sclerosis, and type 1 diabetes, are exposed to the dangerous effects of inflammation, which leads to endothelial dysfunction, early atherosclerosis, and arterial stiffening, causing irreversible damage to blood vessels, heart muscle, and other components of the cardiovascular system. This can result in a higher risk of premature cardiovascular events, such as heart attacks and strokes, in individuals with autoimmune diseases, compared with the general population.

This Special Issue aims to provide a platform for scholars to share their valuable insights on topics such as the prevalence of cardiovascular events and the performance of commonly used cardiovascular risk scores in assessing the risk of future events in patients affected by autoimmune conditions. Further potential topics of interest of this Special Issue include, but are not limited to, the following: the role of inflammation in the development of atherosclerosis; oxidative stress and autoimmunity in atherosclerosis; novel biomarkers of subclinical cardiovascular disease under autoimmune conditions; microbiomes and atherosclerosis in autoimmune diseases; the effects of drugs on cardiovascular disease under autoimmune conditions; and clonal hematopoiesis and cardiovascular disease in autoimmune diseases.

Understanding the mechanisms and risk factors for cardiovascular involvement in autoimmune diseases is crucial for developing effective prevention and treatment strategies to minimize the cardiovascular risk and to protect patients from excessive cardiovascular morbidity and mortality.

We encourage submissions of both original research articles and reviews.

Prof. Dr. Gian Luca Erre
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. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly 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

  • cardiovascular events
  • cardiovascular risk
  • atherosclerosis
  • autoimmune diseases
  • treatment

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Published Papers (2 papers)

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Research

13 pages, 9196 KiB  
Article
Sera from Rheumatoid Arthritis Patients Induce Oxidative Stress and Pro-Angiogenic and Profibrotic Phenotypes in Human Endothelial Cells
by Roberta Giordo, Anna Maria Posadino, Paola Maccioccu, Giampiero Capobianco, Angelo Zinellu, Gian Luca Erre and Gianfranco Pintus
J. Clin. Med. 2024, 13(19), 5913; https://doi.org/10.3390/jcm13195913 - 3 Oct 2024
Viewed by 950
Abstract
Background: Rheumatoid arthritis (RA) is a long-term autoimmune condition marked by persistent inflammation of the joints and various systemic complications, including endothelial dysfunction, atherosclerosis, and pulmonary fibrosis. Oxidative stress is a key contributor to the pathogenesis of RA, potentially exacerbating vascular damage and [...] Read more.
Background: Rheumatoid arthritis (RA) is a long-term autoimmune condition marked by persistent inflammation of the joints and various systemic complications, including endothelial dysfunction, atherosclerosis, and pulmonary fibrosis. Oxidative stress is a key contributor to the pathogenesis of RA, potentially exacerbating vascular damage and promoting pro-angiogenic and profibrotic processes. Objective: This study aims to investigate the effects of sera from RA patients on human umbilical vein endothelial cells (HUVECs), focusing on the induction of oxidative stress, endothelial cell proliferation, migration, and collagen type I synthesis. Methods: Twenty-eight serum samples were collected from RA patients and healthy donors (HDs). HUVECs were exposed to these sera, and intracellular reactive oxygen species (ROS) levels were fluorescently detected using H2DCF-DA. Cell viability was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell migration was evaluated through a scratch wound assay, and collagen type I synthesis was measured using a lentiviral vector expressing the green fluorescent protein (GFP) under the control of the human COL1A1 gene promoter. Results: Exposure to RA sera resulted in a significant increase in intracellular ROS levels in HUVECs compared to HD sera, indicating an elevated state of oxidative stress. RA sera also promoted endothelial cell proliferation and migration, suggesting a pro-angiogenic stimulus. Additionally, RA sera significantly increased collagen type I synthesis in HUVECs, implicating a potential role in profibrotic processes associated with RA. Conclusion: The results of this study emphasize the importance of circulating factors in RA sera in promoting oxidative stress, endothelial dysfunction, and pro-angiogenic and profibrotic phenotypes in endothelial cells. These processes may contribute to the vascular and fibrotic complications observed in RA, highlighting the necessity for additional research into focused therapeutic approaches to alleviate these effects. Full article
(This article belongs to the Special Issue Autoimmune Diseases and Cardiovascular System: Physiopathology, Epidemiology, Clinical Characteristics and Therapeutic Strategies)
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13 pages, 261 KiB  
Article
Real-Life Comparison of Four JAK Inhibitors in Rheumatoid Arthritis (ELECTRA-i Study)
by Maurizio Benucci, Francesca Li Gobbi, Arianna Damiani, Edda Russo, Serena Guiducci, Mariangela Manfredi, Barbara Lari, Valentina Grossi and Maria Infantino
J. Clin. Med. 2024, 13(6), 1821; https://doi.org/10.3390/jcm13061821 - 21 Mar 2024
Cited by 3 | Viewed by 4172
Abstract
Background: Real-world evidence of the efficacy and adverse events of JAK inhibitor treatment (Tofacitinib, Baricitinib, Upadacitinib, and Filgotinib) in rheumatoid arthritis is still limited. Methods: We studied 115 patients from the Rheumatology Unit of S. Giovanni di Dio Hospital affected by D2T-RA, according [...] Read more.
Background: Real-world evidence of the efficacy and adverse events of JAK inhibitor treatment (Tofacitinib, Baricitinib, Upadacitinib, and Filgotinib) in rheumatoid arthritis is still limited. Methods: We studied 115 patients from the Rheumatology Unit of S. Giovanni di Dio Hospital affected by D2T-RA, according to the 2010 EULAR criteria. Out of the 115 patients, 17 had been treated with Baricitinib 8 mg/daily, 32 with Filgotinib 200 mg/daily, 21 with Tofacitinib 10 mg/daily, and 45 with Upadacitinib 15 mg/daily. We evaluated the clinical response after 3, 6, and 12 months of treatment and the follow-up from September 2022 to September 2023. All patients were evaluated according to the number of tender joints (NTJs), number of swollen joints (NSJs), visual analog scale (VAS), global assessment (GA), health assessment questionnaire (HAQ), Disease Activity Score (DAS28), and CDAI. Furthermore, laboratory parameters of efficacy and tolerability were evaluated. Results: All treatments demonstrated a statistically significant decrease in the DAS28 and CDAI scores, tender and swollen joint counts, VAS, HAQ, and patient global assessment (PGA) after 3, 6, and 12 months of treatment. All treatments showed similar behavior, and statistically significant decreases in circulating calprotectin, TNFα, and IL-6 were observed for all drugs after 12 months of treatment. In addition, soluble urokinase plasminogen activator receptor (suPAR) values showed significant differences at baseline and after 12 months of treatment for Filgotinib: 4.87 ± 4.53 vs. 3.61 ± 0.9 (0.009) and Upadacitinib: 6.64 ± 7.12 vs. 4.06 ± 3.61 (0.0003), while no statistically significant differences were found for Baricitinib: 3.4 ± 0.1 vs. 3.78 ± 0.1 and Tofacitinib: 3.95 ± 1.77 vs. 2.58 ± 0.1. The TC/HDL-C ratio (atherogenic index) showed significant differences when comparing Baricitinib vs. Filgotinib (0.0012), Filgotinib vs. Tofacitinib (0.0095), and Filgotinib vs. Upadacitinib (0.0001); furthermore, the LDL-C/HDL-C ratio in the Filgotinib group did not change (2.37 ± 0.45 vs. 2.35 ± 2.13 (NS)) after 12 months of treatment. Venous Thrombotic Events (VTEs) and major adverse cardiovascular events (MACEs) accounted for 1% of adverse events after treatment with Baricitinib. Herpes zoster reactivation accounted for 1% of adverse events after treatment with Filgotinib and Tofacitinib, while non-melanoma skin cancer (NMSC) accounted for 1% of adverse events after Upadacitinib treatment. Conclusions: Our real-world data from patients with RA show differences in some laboratory parameters and in the impact of lipid metabolism in JAK inhibitor treatment. Full article
(This article belongs to the Special Issue Autoimmune Diseases and Cardiovascular System: Physiopathology, Epidemiology, Clinical Characteristics and Therapeutic Strategies)
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