- Department of Gynecology & Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, USAInterests: inflammation and fibrosis; fibrotic disorders; uterine fibroids; hippo signalling; growth factor and progesterone signaling; small molecule inhibitors; and natural compounds
- Assistant Professor of Bioinformatics, Asian University for Women, 20/A M. M. Ali Road, Chattogram, BangladeshInterests: Bioinformatics; the role of Epigenetics (DNA Methylation, Histone Modifications, MicroRNA) in Human Diseases; Inflammation and Fibrosis; and Natural Medicine
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
Manuscripts should be submitted via our online editorial system at https://imr.propub.com by registering and logging in to this website. Once you are registered, click here to start your submission. Manuscripts can be submitted now or up until the deadline. All papers will go through peer-review process. Accepted papers will be published in the journal (as soon as accepted) and meanwhile listed together on the special issue website. Research articles, reviews as well as short communications are preferred. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office to announce on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts will be thoroughly refereed through a double-blind peer-review process. Please visit the Instruction for Authors page before submitting a manuscript. The Article Processing Charge (APC) in this open access journal is 2500 USD. Submitted manuscripts should be well formatted in good English.
- Open Access ReviewSilicosis: New Challenges from an Old Inflammatory and Fibrotic DiseaseClaudia-Mariana Handra, Irina-Luciana Gurzu, Marinela Chirila, Isabel GhitaFront. 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)14Downloads47Views
- Open Access Original Researchβ-arrestin2 Mediates the Arginine Vasopressin-Induced Expression of IL-1β in Murine HeartsNa Yao, Beibei Guo, Yuhang Wang, Ying Hu, ... Weizhong ZhuFront. 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)26Downloads182Views