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10.3390/ijms22126211 http://scihub22266oqcxt.onion/10.3390/ijms22126211 34207510!8226626!34207510     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34207510&cmd=llinks): Failed to open stream: HTTP request failed! 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Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular Mechanisms |pdf=|usr=}}{{34207510}} gab.com Text Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular Mechanisms JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=34207510 #FOAvip Interstitial lung diseases (ILDs) comprise different fibrotic lung disorders characterized by cellular proliferation, interstitial inflammation, and fibrosis. The JAK/STAT molecular pathway is activated under the interaction of a broad number of profibrotic/pro-inflammatory cytokines, such as IL-6, IL-11, and IL-13, among others, which are increased in different ILDs. Similarly, several growth factors over-expressed in ILDs, such as platelet-derived growth factor (PDGF), transforming growth factor beta1 (TGF-beta1), and fibroblast growth factor (FGF) activate JAK/STAT by canonical or non-canonical pathways, which indicates a predominant role of JAK/STAT in ILDs. Between the different JAK/STAT isoforms, it appears that JAK2/STAT3 are predominant, initiating cellular changes observed in ILDs. This review analyzes the expression and distribution of different JAK/STAT isoforms in ILDs lung tissue and different cell types related to ILDs, such as lung fibroblasts and alveolar epithelial type II cells and analyzes JAK/STAT activation. The effect of JAK/STAT phosphorylation on cellular fibrotic processes, such as proliferation, senescence, autophagy, endoplasmic reticulum stress, or epithelial/fibroblast to mesenchymal transition will be described. The small molecules directed to inhibit JAK/STAT activation were assayed in vitro and in in vivo models of pulmonary fibrosis, and different JAK inhibitors are currently approved for myeloproliferative disorders. Recent evidence indicates that JAK inhibitors or monoclonal antibodies directed to block IL-6 are used as compassionate use to attenuate the excessive inflammation and lung fibrosis related to SARS-CoV-2 virus. These altogether indicate that JAK/STAT pathway is an attractive target to be proven in future clinical trials of lung fibrotic disorders. Twit Text FOAVip Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular Mechanisms ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=34207510 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34207510 #FOAvip English Wikipedia <ref>{{Cite pmid|34207510}}</ref> Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular Mechanisms #MMPMID34207510 Montero P; Milara J; Roger I; Cortijo J Int J Mol Sci 2021[Jun]; 22 (12): ä PMID34207510show ga Interstitial lung diseases (ILDs) comprise different fibrotic lung disorders characterized by cellular proliferation, interstitial inflammation, and fibrosis. The JAK/STAT molecular pathway is activated under the interaction of a broad number of profibrotic/pro-inflammatory cytokines, such as IL-6, IL-11, and IL-13, among others, which are increased in different ILDs. Similarly, several growth factors over-expressed in ILDs, such as platelet-derived growth factor (PDGF), transforming growth factor beta1 (TGF-beta1), and fibroblast growth factor (FGF) activate JAK/STAT by canonical or non-canonical pathways, which indicates a predominant role of JAK/STAT in ILDs. Between the different JAK/STAT isoforms, it appears that JAK2/STAT3 are predominant, initiating cellular changes observed in ILDs. This review analyzes the expression and distribution of different JAK/STAT isoforms in ILDs lung tissue and different cell types related to ILDs, such as lung fibroblasts and alveolar epithelial type II cells and analyzes JAK/STAT activation. The effect of JAK/STAT phosphorylation on cellular fibrotic processes, such as proliferation, senescence, autophagy, endoplasmic reticulum stress, or epithelial/fibroblast to mesenchymal transition will be described. The small molecules directed to inhibit JAK/STAT activation were assayed in vitro and in in vivo models of pulmonary fibrosis, and different JAK inhibitors are currently approved for myeloproliferative disorders. Recent evidence indicates that JAK inhibitors or monoclonal antibodies directed to block IL-6 are used as compassionate use to attenuate the excessive inflammation and lung fibrosis related to SARS-CoV-2 virus. These altogether indicate that JAK/STAT pathway is an attractive target to be proven in future clinical trials of lung fibrotic disorders. |Cellular Senescence[MESH] |Endoplasmic Reticulum Stress[MESH] |Humans[MESH] |Interleukins/metabolism[MESH] |Janus Kinases/antagonists & inhibitors/genetics/*metabolism[MESH] |Lung Diseases, Interstitial/drug therapy/metabolism/*pathology[MESH] |Protein Isoforms/genetics/metabolism[MESH] |Protein Kinase Inhibitors/chemistry/metabolism/therapeutic use[MESH] |STAT Transcription Factors/antagonists & inhibitors/genetics/*metabolism[MESH]Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular(epmc).pdf DeepDyve Pubget Overpricing