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Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9.
Oatis, Daniela; Simon-Repolski, Erika; Balta, Cornel; Mihu, Alin; Pieretti, Gorizio; Alfano, Roberto; Peluso, Luisa; Trotta, Maria Consiglia; D'Amico, Michele; Hermenean, Anca.
  • Oatis D; Department of Infectious Disease, Faculty of Medicine, Vasile Goldis Western University of Arad, 310414 Arad, Romania.
  • Simon-Repolski E; Doctoral School of Biology, Vasile Goldis Western University of Arad, 310414 Arad, Romania.
  • Balta C; Doctoral School of Medicine, Vasile Goldis Western University of Arad, 310414 Arad, Romania.
  • Mihu A; Department of Pneumology, Arad Clinical Emergency Hospital, 310031 Arad, Romania.
  • Pieretti G; "Aurel Ardelean" Institute of Life Sciences, Vasile Goldis Western University of Arad, 310144 Arad, Romania.
  • Alfano R; Department of Microbiology, Faculty of Medicine, Vasile Goldis Western University of Arad, 310414 Arad, Romania.
  • Peluso L; Department of Plastic Surgery, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy.
  • Trotta MC; Department of Advanced Medical and Surgical Sciences "DAMSS", University of Campania "Luigi Vanvitelli", 80138 Naples, Italy.
  • D'Amico M; Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy.
  • Hermenean A; Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", 80138 Naples, Italy.
Int J Mol Sci ; 23(15)2022 Jul 26.
Article in English | MEDLINE | ID: covidwho-1957349
ABSTRACT
Pulmonary fibrosis is a consequence of the pathological accumulation of extracellular matrix (ECM), which finally leads to lung scarring. Although the pulmonary fibrogenesis is almost known, the last two years of the COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its post effects added new particularities which need to be explored. Many questions remain about how pulmonary fibrotic changes occur within the lungs of COVID-19 patients, and whether the changes will persist long term or are capable of resolving. This review brings together existing knowledge on both COVID-19 and pulmonary fibrosis, starting with the main key players in promoting pulmonary fibrosis, such as alveolar and endothelial cells, fibroblasts, lipofibroblasts, and macrophages. Further, we provide an overview of the main molecular mechanisms driving the fibrotic process in connection with Galactin-1, -3, -8, and -9, together with the currently approved and newly proposed clinical therapeutic solutions given for the treatment of fibrosis, based on their inhibition. The work underlines the particular pathways and processes that may be implicated in pulmonary fibrosis pathogenesis post-SARS-CoV-2 viral infection. The recent data suggest that galectin-1, -3, -8, and -9 could become valuable biomarkers for the diagnosis and prognosis of lung fibrosis post-COVID-19 and promising molecular targets for the development of new and original therapeutic tools to treat the disease.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Pulmonary Fibrosis / COVID-19 Type of study: Prognostic study Topics: Long Covid Limits: Humans Language: English Year: 2022 Document Type: Article Affiliation country: Ijms23158210

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Pulmonary Fibrosis / COVID-19 Type of study: Prognostic study Topics: Long Covid Limits: Humans Language: English Year: 2022 Document Type: Article Affiliation country: Ijms23158210