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Current Molecular Medicine

Editor-in-Chief

ISSN (Print): 1566-5240
ISSN (Online): 1875-5666

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Editorial

Fibrosis: From Cellular and Molecular Targets to Therapeutic Strategies

Author(s): Chiara Sassoli

Volume 22, Issue 3, 2022

Published on: 14 March, 2022

Page: [193 - 195] Pages: 3

DOI: 10.2174/156652402203220314140908

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[1]
Rosenbloom J, Macarak E, Piera-Velazquez S, Jimenez SA. Human Fibrotic Diseases: Current Challenges in Fibrosis Research. Methods Mol Biol 2017; 1627: 1-23.
[http://dx.doi.org/10.1007/978-1-4939-7113-8_1.] [PMID: 28836191]
[2]
Weiskirchen R, Weiskirchen S, Tacke F. Organ and tissue fibrosis: Molecular signals, cellular mechanisms and translational implications. Mol Aspects Med 2019; 65: 2-15.
[http://dx.doi.org/10.1016/j.mam.2018.06.003] [PMID: 29958900]
[3]
Miao H, Wu XQ, Zhang DD, Wang YN, Guo Y, Li P, et al. Deciphering the cellular mechanisms underlying fibrosis-associated diseases and therapeutic avenues. Pharmacological Research 2021; 163: 105316.
[http://dx.doi.org/10.1016/j.phrs.2020.105316] [PMID: 33248198]
[4]
Zeisberg M, Kalluri R. Cellular mechanisms of tissue fibrosis. 1. Common and organ-specific mechanisms associated with tissue fibrosis. Am J Physiol Cell Physiol 2013; 304(3): C216-25.
[http://dx.doi.org/10.1152/ajpcell.00328.201223255577] [PMID: 23255577]
[5]
Pakshir P, Hinz B. The big five in fibrosis: Macrophages, myofibroblasts, matrix, mechanics, and miscommunication. Matrix Biol 2018; 68-69: 81-93.
[http://dx.doi.org/10.1016/j.matbio.2018.01.019] [PMID: 29408013]
[6]
Squecco R, Sassoli C, Garella R, et al. Inhibitory effects of relaxin on cardiac fibroblast-to-myofibroblast transition: an electrophysiological study. Exp Physiol 2015; 100(6): 652-66.
[http://dx.doi.org/10.1113/EP085178.] [PMID: 25786395]
[7]
Sassoli C, Chellini F, Squecco R, et al. Low intensity 635 nm diode laser irradiation inhibits fibroblast-myofibroblast transition reducing TRPC1 channel expression/activity: New perspectives for tissue fibrosis treatment. Lasers Surg Med 2016; 48(3): 318-32.
[http://dx.doi.org/10.1002/lsm.22441] [PMID: 26660509]
[8]
Pakshir P, Noskovicova N, Lodyga M, et al. The myofibroblast at a glance. J Cell Sci 2020; 133(13): jcs227900.
[http://dx.doi.org/10.1242/jcs.227900.] [PMID: 32651236]
[9]
Squecco R, Chellini F, Idrizaj E, et al. Platelet-rich plasma modulates gap junction functionality and connexin 43 and 26 expression during TGF-β1-induced fibroblast to myofibroblast transition: clues for counteracting fibrosis. Cells 2020; 9(5): 1199.
[http://dx.doi.org/10.3390/cells9051199] [PMID: 32408529]
[10]
Sassoli C, Garella R, Chellini F, et al. Platelet-rich plasma affects gap junctional features in myofibroblasts in vitro via vascular endothelial growth factor (VEGF)-A/VEGF receptor. Exp Physiol 2022; 107(2): 106-21.
[http://dx.doi.org/10.1113/EP090052.] [PMID: 34935228]
[11]
Van De Water L, Varney S, Tomasek JJ. Mechanoregulation of the myofibroblast in wound contraction, scarring, and fibrosis: opportunities for new therapeutic intervention. Adv Wound Care 2013; 2: 122-41.
[http://dx.doi.org/10.1089/wound.2012.0393.] [PMID: 24527336]
[12]
Eming SA, Wynn TA, Martin P. Inflammation and metabolism in tissue repair and regeneration. Science 2017; 356(6342): 1026-30.
[http://dx.doi.org/10.1126/science.aam7928.] [PMID: 28596335]
[13]
Kalluri R, Weinberg RA. The basics of epithelial- mesenchymal transition. J Clin Invest 2009; 119(6): 1420-8.
[http://dx.doi.org/10.1172/JCI39104] [PMID: 19487818]
[14]
Brenner DA, Kisseleva T, Scholten D, et al. Origin of myofibroblasts in liver fibrosis. Fibrogenesis Tissue Repair 2012; 5(Suppl. 1): S17.
[http://dx.doi.org/10.1186/1755-1536-5-S1-S17] [PMID: 23259769]
[15]
LeBleu VS, Taduri G, O’Connell J, et al. Origin and function of myofibroblasts in kidney fibrosis. Nat Med 2013; 19(8): 1047-53.
[http://dx.doi.org/10.1038/nm.3218] [PMID: 23817022]
[16]
Piera-Velazquez S, Jimenez SA. Endothelial to Mesenchymal Transition: Role in Physiology and in the Pathogenesis of Human Diseases. Physiol Rev 2019; 99: 1281-324.
[http://dx.doi.org/10.1152/physrev.00021.2018] [PMID: 30864875]
[17]
Hannan RT, Miller AE, Hung RC, Sano C, Peirce SM, Barker TH. Extracellular matrix remodeling associated with bleomycin-induced lung injury supports pericyte-to-myofibroblast transition. Matrix Biol Plus 2020; 10: 100056.
[http://dx.doi.org/10.1016/j.mbplus.2020.100056.] [PMID: 34195593]
[18]
Tai Y, Woods EL, Dally J, et al. Myofibroblasts: Function, Formation, and Scope of Molecular Therapies for Skin Fibrosis. Biomolecules 2021; 11(8): 1095.
[http://dx.doi.org/10.3390/biom11081095.] [PMID: 34439762]
[19]
Sassoli C, Nistri S, Chellini F, Bani D. Human Recombinant Relaxin (Serelaxin) as Anti-fibrotic Agent: Pharmacology, Limitations and Actual Perspectives. Curr Mol Med 2021; 3: 196-208.
[http://dx.doi.org/10.2174/1566524021666210309113650] [PMID: 33687895]
[20]
Romano E, Rosa I, Fioretto BS, Cerinic MM, Manetti M. The Role of Pro-fibrotic Myofibroblasts in Systemic Sclerosis: from Origin to Therapeutic Targeting. Curr Mol Med 2021; 3: 209-39.
[http://dx.doi.org/10.2174/0929867328666210325102749] [PMID: 33823766]
[21]
Pinar A, Samuel CS. Immune Mechanisms and Related Targets for the Treatment of Fibrosis in Various Organs. Curr Mol Med 2022; 3: 240-9.
[22]
Sharma AR, Sharma G, Bhattacharya M, Lee SS, Chakraborty C. Circulating miRNA in atherosclerosis: a clinical biomarker and early diagnostic tool. Curr Mol Med 2021; 3: 250-62.
[http://dx.doi.org/10.2174/1566524021666210315124438] [PMID: 33719955]

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