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Cellular Mechanisms and Signaling Pathways in Normal Tissue Repair and Fibrosis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 29 June 2025 | Viewed by 229

Special Issue Editors


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Guest Editor
Department of Pharmacology, The Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814, USA
Interests: cell biology and signal transduction of normal tissue repair and fibrotic remodeling in the lung; adult stem cells that participate in lung repair; apoptosis; cytoskeletal rearrangement; cellular senescence and inflammation; reactive oxygen species in signal transduction and antioxidant cellular defenses
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Guest Editor
Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Interests: fibrotic lung disease; pulmonary injury; bioinformatics; animal models; COPD

Special Issue Information

Dear Colleagues,

Fibrotic disorders have been described for all organs, including the heart, liver, kidney, lung, spleen, pancreas, thymus, lymph nodes, bone marrow, brain, skin, gastrointestinal tract, eyes, etc. For many of these organs, the events initiating fibrosis are not well defined, although in some cases, the process appears to involve inflammation and/or tissue injury followed by failed repair, ultimately resulting in fibrotic remodeling. For many of these diseases, fibrosis is progressive, and reversal of fibrosis to form functional tissue has not been described. Recent research describes novel molecular and biochemical pathways involved in fibrotic remodeling and the development of animal models that recapitulate the human diseases.

For this Special Issue, we would like to invite papers that investigate molecular and cellular mechanisms for the initiation and progression of fibrosis and the discovery of antifibrotics. Some potential topics include:

  1. The relationship between inflammation/inflammatory responses and fibrotic remodeling.
  2. The accelerated senescence or loss of adult stem cells in a tissue and the activation of fibrotic remodeling as a response to loss of normal tissue turnover.
  3. The activation of novel signaling pathways that may initiate or perpetuate fibrosis and inhibit normal tissue repair.
  4. Novel animal models for the testing and development of antifibrotic agents.
  5. Agents that delay, suppress, or reverse fibrotic remodeling.

This Special Issue is calling for both original articles and reviews providing to the readers of IJMS comprehensive reviews of fibrosis pathways in any one organ system or a comparison of fibrotic pathways in multiple organs, highlighting similarities and differences.

Prof. Dr. Regina M. Day
Dr. Jeffrey R. Koenitzer
Guest Editors

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Keywords

  • fibrosis
  • inflammation
  • senescence
  • myofibroblasts
  • Wnt/hedgehog
  • extracellular matrix
  • hedgehog
  • angiotensin II/transforming growth factor-beta
  • ephrins

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Published Papers (1 paper)

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Research

18 pages, 4066 KiB  
Article
Furosemide Promotes Inflammatory Activation and Myocardial Fibrosis in Swine with Tachycardia-Induced Heart Failure
by Nisha Plavelil, Robert Goldstein, Michael G. Klein, Luke Michaelson, Mark C. Haigney and Maureen N. Hood
Int. J. Mol. Sci. 2025, 26(13), 6088; https://doi.org/10.3390/ijms26136088 - 25 Jun 2025
Viewed by 66
Abstract
Loop diuretics like furosemide are commonly used in heart failure (HF) treatment, but their effects on disease progression are still unclear. Furosemide treatment accelerates HF deterioration in a swine model, but the mechanism of acceleration is poorly understood. We hypothesized that furosemide activates [...] Read more.
Loop diuretics like furosemide are commonly used in heart failure (HF) treatment, but their effects on disease progression are still unclear. Furosemide treatment accelerates HF deterioration in a swine model, but the mechanism of acceleration is poorly understood. We hypothesized that furosemide activates inflammatory signaling in the failing left ventricular (LV) myocardium, leading to adverse remodeling of the extracellular matrix (ECM). A total of 14 Yorkshire pigs underwent permanent transvenous pacemaker implantation and were paced at 200 beats per minute; 9 non-instrumented pigs provided controls. Seven paced animals received normal saline, and seven received furosemide at a dose of 1 mg/kg intramuscularly. Weekly echocardiograms were performed. Furosemide-treated animals reached the HF endpoint a mean of 3.2 days sooner than saline-treated controls (mean 28.9 ± 3.8 SEM for furosemide and 32.1 ± 2.5 SEM for saline). The inflammatory signaling protein transforming growth factor-beta (TGF-β) and its downstream proteins were significantly (p ≤ 0.05) elevated in the LV after furosemide treatment. The regulatory factors in cell proliferation, mitogen-activated protein kinase signaling pathway proteins, and matrix metalloproteinases were elevated in the furosemide-treated animals (p ≤ 0.05). Our data showed that furosemide treatment increased ECM remodeling and myocardial fibrosis, reflecting increased TGF-β signaling factors, supporting prior results showing worsened HF. Full article
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