Inflammation and fibrosis: from molecular mechanisms to therapeutic opportunities
Submission Deadline: 31 Mar 2023
Guest Editors

Department of Gynecology & Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
Interests: inflammation and fibrosis; fibrotic disorders; uterine fibroids; Hippo/YAP signaling; growth factors; activin A and TGF-β; myofibroblasts; ECM Remodeling; small molecule inhibitors; anti-fibrotic compounds
Special Issue in IMR Press journals

Science and Math Program, Asian University for Women, Chattogram, Bangladesh
Interests: microRNA; extracellular matrix; bioinformatics; inflammation; pathological fibrosis; cancers
Special Issue in IMR Press journals
Special Issue Information
Dear Colleadues,
Inflammation and fibrosis are critical pathological processes involved in many human diseases. These include inflammatory pulmonary fibrosis, uterine fibroids, kidney fibrosis, liver fibrosis, cardiac fibrosis, pancreas fibrosis, hypertrophic/keloid scars, scleroderma and systemic sclerosis, dupuytren’s and peyronie’s disease, atherosclerosis and acute coronary syndromes, as well as many tumors and cancers. Inflammation is the body’s first response to injury. Fibrosis is the result of defective repair processes often seen after chronic injury and/or inflammation that is associated with excessive accumulation of ECM proteins leading to disruption of normal tissue architecture.
Quiescent cells are activated by tissue injury, and/or inflammation. Cytokines, chemokines, and growth factors are produced at the site of injury and contribute to fibroblast activation and differentiation into myofibroblasts. Angiogenic growth factors also take part in this process. To restore homeostatic condition, myofibroblasts produce ECM proteins and maintain MMPs (matrix metalloproteinases)-TIMPs (inhibitors of metalloproteinases) balance, resulting in wound healing and myofibroblasts are eliminated by apoptosis. However, under a chronic inflammatory state, myofibroblasts become resistant to apoptosis, producing excessive amounts of ECM proteins, and therefore MMP-TIMP imbalance which induces cells to undergo fibrotic transformation.
In recent years, significant progress has been made in the understanding of the contribution of inflammation and fibrosis in human diseases as well as the development of new therapeutic compounds. Therefore, the purpose of this special issue of Frontiers in Bioscience-Landmark is to collect original research articles and reviews on the role of inflammation and fibrosis in human diseases as well as the current status of therapeutic compounds (from natural to synthetic compounds) that target inflammation and fibrosis.
Md Soriful Islam and Most Mauluda Akhtar
Guest Editors
Keywords
- Inflammation
- Inflammatory Conditions
- Fibrosis
- Fibrotic Diseases
- Tumors
- Cancers
- Cellular Signaling Pathways
- Anti-Inflammatory Compounds
- Antifibrotic Compounds
- Anticancer Compounds
- Natural Compounds
- Small Molecule Inhibitors
Published Papers (5)
MicroRNA in Fibrotic Disorders: A Potential Target for Future Therapeutics
Front. Biosci. (Landmark Ed) 2023, 28(11), 317; https://doi.org/10.31083/j.fbl2811317
(This article belongs to the Special Issue Inflammation and fibrosis: from molecular mechanisms to therapeutic opportunities)
Serum Pentaxin 3 (PTX3) Promotes NLRP3 Inflammasome and Pyroptosis in Patients with Up-Regulated Myasthenia Gravis
Front. Biosci. (Landmark Ed) 2023, 28(11), 306; https://doi.org/10.31083/j.fbl2811306
(This article belongs to the Special Issue Inflammation and fibrosis: from molecular mechanisms to therapeutic opportunities)
Potential Therapeutic Targets of Resveratrol in the Prevention and Treatment of Pulmonary Fibrosis
Front. Biosci. (Landmark Ed) 2023, 28(9), 198; https://doi.org/10.31083/j.fbl2809198
(This article belongs to the Special Issue Inflammation and fibrosis: from molecular mechanisms to therapeutic opportunities)
Silicosis: New Challenges from an Old Inflammatory and Fibrotic Disease
Front. Biosci. (Landmark Ed) 2023, 28(5), 96; https://doi.org/10.31083/j.fbl2805096
(This article belongs to the Special Issue Inflammation and fibrosis: from molecular mechanisms to therapeutic opportunities)
β-arrestin2 Mediates the Arginine Vasopressin-Induced Expression of IL-1β in Murine Hearts
Front. Biosci. (Landmark Ed) 2023, 28(1), 7; https://doi.org/10.31083/j.fbl2801007
(This article belongs to the Special Issue Inflammation and fibrosis: from molecular mechanisms to therapeutic opportunities)
