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10th Anniversary of Biomedicines—from Inflammation to Fibrosis: Implications of...
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10th Anniversary of Biomedicines—from Inflammation to Fibrosis: Implications of Human Diseases

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 July 2023) | Viewed by 7035

Special Issue Editor

Dr. Dong Kwon Yang

E-Mail Website
Guest Editor
Department of Veterinary Pharmacology and Toxicology, College of Veterinary Medicine, Jeonbuk National University, Iksan 54596, Korea
Interests: cardiovascular diseases; oxidative stress; mitochondria; natural compounds; diabetes; liver toxicity; animal models of diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammation is an important trigger for regeneration and fibrosis following tissue damage. Inflammation is a physiological defense mechanism of the body against many pathological stimuli. However, the inflammatory response is extremely complex and comprises several stages. Fibrosis is closely associated with inflammation and is an essential component of tissue repair that follows tissue injury. Therefore, fibrosis reflects a pathologic state resulting in impairment of function and organ damage. In particular, inflammation and fibrosis are implicated in various human diseases, such as cardiovascular diseases, liver diseases, and so on. Therefore, they are considered to be therapeutic options to prevent disease progression to organ dysfunction.

This Special Issue will discuss research findings or reviews highlighting the role of inflammation and fibrosis in various human diseases, and aims to bring together current knowledge of the mechanisms and pathways involved in incidence and action of inflammation and fibrosis in human diseases. Additionally, we also welcome the submission of research on the mechanisms and actions of novel therapeutic targets against inflammation and fibrosis in strategies to modulate them in human diseases.

Dr. Dong Kwon Yang
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

  • inflammation
  • fibrosis, cardiovascular diseases
  • liver diseases
  • fibrotic biomarker
  • therapeutic target

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Related Special Issue

Published Papers (4 papers)

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11 pages, 1734 KiB  
Article
Non-Neuronal Acetylcholinesterase Activity Shows Limited Utility for Early Detection of Sepsis
by Aleksandar R. Zivkovic, Karsten Schmidt, Stefan Hofer, Thorsten Brenner, Markus A. Weigand and Sebastian O. Decker
Biomedicines 2023, 11(8), 2111; https://doi.org/10.3390/biomedicines11082111 - 26 Jul 2023
Viewed by 1100
Abstract
(1) Background: Sepsis is a severe systemic inflammatory condition characterized by rapid clinical deterioration and organ dysfunction. The cholinergic system has been implicated in modulating the inflammatory response. Acetylcholinesterase (AChE), an enzyme primarily responsible for the hydrolysis of acetylcholine, has been proposed as [...] Read more.
(1) Background: Sepsis is a severe systemic inflammatory condition characterized by rapid clinical deterioration and organ dysfunction. The cholinergic system has been implicated in modulating the inflammatory response. Acetylcholinesterase (AChE), an enzyme primarily responsible for the hydrolysis of acetylcholine, has been proposed as a potential early indicator of sepsis onset. However, the exact role of non-neuronal AChE activity in sepsis and its correlation with disease severity and patient outcomes remain unclear. This study aimed to investigate the involvement of AChE activity in sepsis and evaluate its association with disease severity and clinical outcomes. (2) Methods: A prospective study included 43 septic patients. AChE activity was measured at sepsis detection, as well as 7 and 28 days later. Inflammatory biomarkers, disease severity scores, and patient outcomes were evaluated. (3) Results: AChE activity remained stable for 7 days and decreased at 28 days. However, there was no correlation between initial AChE activity and inflammatory biomarkers, disease severity scores, ICU stay, or hospital stay. (4) Conclusions: Non-neuronal AChE activity may not reliably indicate early sepsis or predict disease severity. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines—from Inflammation to Fibrosis: Implications of Human Diseases)
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11 pages, 3940 KiB  
Article
Fusion Protein of RBP and Albumin Domain III Reduces Lung Fibrosis by Inactivating Lung Stellate Cells
by Jaeho Choi, Yuna Son, Ji Wook Moon, Dae Won Park, Young-Sik Kim and Junseo Oh
Biomedicines 2023, 11(7), 2007; https://doi.org/10.3390/biomedicines11072007 - 16 Jul 2023
Cited by 2 | Viewed by 1608
Abstract
Activated stellate cells play a role in fibrosis development in the liver, pancreas, and kidneys. The fusion protein R-III, which consists of retinol-binding protein and albumin domain III, has been demonstrated to attenuate liver and renal fibrosis by suppressing stellate cell activation. In [...] Read more.
Activated stellate cells play a role in fibrosis development in the liver, pancreas, and kidneys. The fusion protein R-III, which consists of retinol-binding protein and albumin domain III, has been demonstrated to attenuate liver and renal fibrosis by suppressing stellate cell activation. In this study, we investigated the efficacy of R-III against bleomycin-induced lung fibrosis in mice. R-III reduced lung fibrosis and primarily localized in autofluorescent cells in the lung tissue. Furthermore, we isolated lung stellate cells (LSCs) from rat lungs using the isolation protocol employed for hepatic stellate cells (HSCs). LSCs shared many characteristics with HSCs, including the presence of vitamin A-containing lipid droplets and the expression of alpha-smooth muscle actin and collagen type I, markers for activated HSCs/myofibroblasts. LSCs spontaneously transdifferentiated into myofibroblasts in in vitro culture, which was inhibited by R-III. These findings suggest that R-III may reduce lung fibrosis by inactivating LSCs and could be a promising treatment for extrahepatic fibrosis. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines—from Inflammation to Fibrosis: Implications of Human Diseases)
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12 pages, 591 KiB  
Article
FIB-4 Index and Neutrophil-to-Lymphocyte-Ratio as Death Predictor in Coronary Artery Disease Patients
by Melania Gaggini, Fabrizio Minichilli, Francesca Gorini, Serena Del Turco, Patrizia Landi, Alessandro Pingitore and Cristina Vassalle
Biomedicines 2023, 11(1), 76; https://doi.org/10.3390/biomedicines11010076 - 28 Dec 2022
Cited by 2 | Viewed by 1926
Abstract
Nonalcoholic fatty liver disease (NAFLD)-associated liver fibrosis is likely related to coronary artery disease (CAD) by the mediation of systemic inflammation. This study aimed at evaluating the predictive value of neutrophil-to-lymphocyte-ratio (NLR) and fibrosis-4 index (FIB-4), indices of inflammation and fibrosis, respectively, on [...] Read more.
Nonalcoholic fatty liver disease (NAFLD)-associated liver fibrosis is likely related to coronary artery disease (CAD) by the mediation of systemic inflammation. This study aimed at evaluating the predictive value of neutrophil-to-lymphocyte-ratio (NLR) and fibrosis-4 index (FIB-4), indices of inflammation and fibrosis, respectively, on CAD mortality. Data from 1460 CAD patients (1151 males, age: 68 ± 10 years, mean ± SD) were retrospectively analyzed. Over a median follow-up of 26 months (interquartile range (IQR) 12–45), 94 deaths were recorded. Kaplan–Meier survival analysis revealed worse outcomes in patients with elevation of one or both biomarkers (FIB-4 > 3.25 or/and NLR > 2.04, log-rank p-value < 0.001). In multivariate Cox regression analysis, the elevation of one biomarker (NLR or FIB-4) still confers a significant independent risk for mortality (hazard ratio (HR) = 1.7, 95% confidence interval (95% CI): 1.1–2.7, p = 0.023), whereas an increase in both biomarkers confers a risk corresponding to HR = 3.5 (95% CI: 1.6–7.8, p = 0.002). Categorization of patients with elevated FIB-4/NLR could provide valuable information for risk stratification and reduction of residual risk in CAD patients. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines—from Inflammation to Fibrosis: Implications of Human Diseases)
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11 pages, 1272 KiB  
Perspective
Spontaneous Epiretinal Membrane Resolution and Angiotensin Receptor Blockers: Case Observation, Literature Review and Perspectives
by Filippo Confalonieri, Xhevat Lumi and Goran Petrovski
Biomedicines 2023, 11(7), 1976; https://doi.org/10.3390/biomedicines11071976 - 12 Jul 2023
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Abstract
Introduction: Epiretinal membrane (ERM) is a relatively common condition affecting the macula. When symptoms become apparent and compromise a patient’s quality of vision, the only therapeutic approach available today is surgery with a vitrectomy and peeling of the ERM. Angiotensin receptor blockers (ARBs) [...] Read more.
Introduction: Epiretinal membrane (ERM) is a relatively common condition affecting the macula. When symptoms become apparent and compromise a patient’s quality of vision, the only therapeutic approach available today is surgery with a vitrectomy and peeling of the ERM. Angiotensin receptor blockers (ARBs) and angiotensin-converting enzyme inhibitors (ACE-Is) reduce the effect of angiotensin II, limit the amount of fibrosis, and demonstrate consequences on fibrinogenesis in the human body. Case Description and Materials and Methods: A rare case of spontaneous ERM resolution with concomitant administration of ARB is reported. The patient was set on ARB treatment for migraines and arterial hypertension, and a posterior vitreous detachment was already present at the first diagnosis of ERM. The scientific literature addressing the systemic relationship between ARB, ACE-Is, and fibrosis in the past 25 years was searched in the PubMed, Medline, and EMBASE databases. Results: In total, 38 and 16 original articles have been selected for ARBs and ACE-Is, respectively, in regard to fibrosis modulation. Conclusion: ARBs and ACE-Is might have antifibrotic activity on ERM formation and resolution. Further clinical studies are necessary to explore this phenomenon. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines—from Inflammation to Fibrosis: Implications of Human Diseases)
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