Effect of antibody-mediated connective tissue growth factor neutralization on lung edema in ventilator-induced lung injury in rats

Background Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in...

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Vydáno v:Molecular medicine (Cambridge, Mass.) Ročník 30; číslo 1; s. 68 - 11
Hlavní autoři: van den Brom, Charissa E., Bozic, Caitlin, Polet, Chantal A., Bongers, Annabel, Tuip-de Boer, Anita M., Ibelings, Roselique, Roelofs, Joris J. T. H., Juffermans, Nicole P.
Médium: Journal Article
Jazyk:angličtina
Vydáno: London BioMed Central 22.05.2024
Springer Nature B.V
BMC
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ISSN:1528-3658, 1076-1551, 1528-3658
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Abstract Background Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI. Methods Following LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low V T ) or moderate (10 mL/kg; mod V T ) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low V T . Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined. Results VILI was characterized by reduced PaO 2 /FiO 2 ratio (low V T : 540 [381–661] vs. control: 693 [620–754], p < 0.05), increased wet-to-dry weight ratio (low V T : 4.8 [4.6–4.9] vs. control: 4.5 [4.4–4.6], p < 0.05), pneumonia (low V T : 30 [0–58] vs. control: 0 [0–0]%, p < 0.05) and interstitial inflammation (low V T : 2 [1–3] vs. control: 1 [0–1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod V T  + FG-3154: 4.8 [4.7–5.0] vs. mod V T  + vehicle: 4.8 [4.8–5.0], p > 0.99), extravasated dextrans (mod V T  + FG-3154: 0.06 [0.04–0.09] vs. mod V T  + vehicle: 0.04 [0.03–0.09] µg/mg tissue, p > 0.99), sRAGE (mod V T  + FG-3154: 1865 [1628–2252] vs. mod V T  + vehicle: 1885 [1695–2159] pg/mL, p > 0.99) or histopathology. Conclusions ‘Double hit’ VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI. Graphical Abstract
AbstractList Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI.BACKGROUNDAcute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI.Following LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low VT) or moderate (10 mL/kg; mod VT) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low VT. Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined.METHODSFollowing LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low VT) or moderate (10 mL/kg; mod VT) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low VT. Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined.VILI was characterized by reduced PaO2/FiO2 ratio (low VT: 540 [381-661] vs. control: 693 [620-754], p < 0.05), increased wet-to-dry weight ratio (low VT: 4.8 [4.6-4.9] vs. control: 4.5 [4.4-4.6], p < 0.05), pneumonia (low VT: 30 [0-58] vs. control: 0 [0-0]%, p < 0.05) and interstitial inflammation (low VT: 2 [1-3] vs. control: 1 [0-1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod VT + FG-3154: 4.8 [4.7-5.0] vs. mod VT + vehicle: 4.8 [4.8-5.0], p > 0.99), extravasated dextrans (mod VT + FG-3154: 0.06 [0.04-0.09] vs. mod VT + vehicle: 0.04 [0.03-0.09] µg/mg tissue, p > 0.99), sRAGE (mod VT + FG-3154: 1865 [1628-2252] vs. mod VT + vehicle: 1885 [1695-2159] pg/mL, p > 0.99) or histopathology.RESULTSVILI was characterized by reduced PaO2/FiO2 ratio (low VT: 540 [381-661] vs. control: 693 [620-754], p < 0.05), increased wet-to-dry weight ratio (low VT: 4.8 [4.6-4.9] vs. control: 4.5 [4.4-4.6], p < 0.05), pneumonia (low VT: 30 [0-58] vs. control: 0 [0-0]%, p < 0.05) and interstitial inflammation (low VT: 2 [1-3] vs. control: 1 [0-1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod VT + FG-3154: 4.8 [4.7-5.0] vs. mod VT + vehicle: 4.8 [4.8-5.0], p > 0.99), extravasated dextrans (mod VT + FG-3154: 0.06 [0.04-0.09] vs. mod VT + vehicle: 0.04 [0.03-0.09] µg/mg tissue, p > 0.99), sRAGE (mod VT + FG-3154: 1865 [1628-2252] vs. mod VT + vehicle: 1885 [1695-2159] pg/mL, p > 0.99) or histopathology.'Double hit' VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI.CONCLUSIONS'Double hit' VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI.
BackgroundAcute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI.MethodsFollowing LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low VT) or moderate (10 mL/kg; mod VT) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low VT. Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined.ResultsVILI was characterized by reduced PaO2/FiO2 ratio (low VT: 540 [381–661] vs. control: 693 [620–754], p < 0.05), increased wet-to-dry weight ratio (low VT: 4.8 [4.6–4.9] vs. control: 4.5 [4.4–4.6], p < 0.05), pneumonia (low VT: 30 [0–58] vs. control: 0 [0–0]%, p < 0.05) and interstitial inflammation (low VT: 2 [1–3] vs. control: 1 [0–1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod VT + FG-3154: 4.8 [4.7–5.0] vs. mod VT + vehicle: 4.8 [4.8–5.0], p > 0.99), extravasated dextrans (mod VT + FG-3154: 0.06 [0.04–0.09] vs. mod VT + vehicle: 0.04 [0.03–0.09] µg/mg tissue, p > 0.99), sRAGE (mod VT + FG-3154: 1865 [1628–2252] vs. mod VT + vehicle: 1885 [1695–2159] pg/mL, p > 0.99) or histopathology.Conclusions‘Double hit’ VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI.
Abstract Background Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI. Methods Following LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low VT) or moderate (10 mL/kg; mod VT) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low VT. Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined. Results VILI was characterized by reduced PaO2/FiO2 ratio (low VT: 540 [381–661] vs. control: 693 [620–754], p < 0.05), increased wet-to-dry weight ratio (low VT: 4.8 [4.6–4.9] vs. control: 4.5 [4.4–4.6], p < 0.05), pneumonia (low VT: 30 [0–58] vs. control: 0 [0–0]%, p < 0.05) and interstitial inflammation (low VT: 2 [1–3] vs. control: 1 [0–1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod VT + FG-3154: 4.8 [4.7–5.0] vs. mod VT + vehicle: 4.8 [4.8–5.0], p > 0.99), extravasated dextrans (mod VT + FG-3154: 0.06 [0.04–0.09] vs. mod VT + vehicle: 0.04 [0.03–0.09] µg/mg tissue, p > 0.99), sRAGE (mod VT + FG-3154: 1865 [1628–2252] vs. mod VT + vehicle: 1885 [1695–2159] pg/mL, p > 0.99) or histopathology. Conclusions ‘Double hit’ VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI. Graphical Abstract
Background Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI. Methods Following LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low V T ) or moderate (10 mL/kg; mod V T ) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low V T . Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined. Results VILI was characterized by reduced PaO 2 /FiO 2 ratio (low V T : 540 [381–661] vs. control: 693 [620–754], p < 0.05), increased wet-to-dry weight ratio (low V T : 4.8 [4.6–4.9] vs. control: 4.5 [4.4–4.6], p < 0.05), pneumonia (low V T : 30 [0–58] vs. control: 0 [0–0]%, p < 0.05) and interstitial inflammation (low V T : 2 [1–3] vs. control: 1 [0–1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod V T  + FG-3154: 4.8 [4.7–5.0] vs. mod V T  + vehicle: 4.8 [4.8–5.0], p > 0.99), extravasated dextrans (mod V T  + FG-3154: 0.06 [0.04–0.09] vs. mod V T  + vehicle: 0.04 [0.03–0.09] µg/mg tissue, p > 0.99), sRAGE (mod V T  + FG-3154: 1865 [1628–2252] vs. mod V T  + vehicle: 1885 [1695–2159] pg/mL, p > 0.99) or histopathology. Conclusions ‘Double hit’ VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI. Graphical Abstract
Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung injury, termed ventilator-induced lung injury (VILI). Connective tissue growth factor (CTGF), a mediator of fibrosis, is increased in ARDS patients. Blocking CTGF inhibits fibrosis and possibly vascular leakage. This study investigated whether neutralizing CTGF reduces pulmonary edema in VILI. Following LPS administration, rats were mechanically ventilated for 6 h with low (6 mL/kg; low V ) or moderate (10 mL/kg; mod V ) tidal volume and treated with a neutralizing CTGF antibody (FG-3154) or placebo lgG (vehicle). Control rats without LPS were ventilated for 6 h with low V . Lung wet-to-dry weight ratio, FITC-labeled dextran permeability, histopathology, and soluble RAGE were determined. VILI was characterized by reduced PaO /FiO ratio (low V : 540 [381-661] vs. control: 693 [620-754], p < 0.05), increased wet-to-dry weight ratio (low V : 4.8 [4.6-4.9] vs. control: 4.5 [4.4-4.6], p < 0.05), pneumonia (low V : 30 [0-58] vs. control: 0 [0-0]%, p < 0.05) and interstitial inflammation (low V : 2 [1-3] vs. control: 1 [0-1], p < 0.05). FG-3154 did not affect wet-to-dry weight ratio (mod V  + FG-3154: 4.8 [4.7-5.0] vs. mod V  + vehicle: 4.8 [4.8-5.0], p > 0.99), extravasated dextrans (mod V  + FG-3154: 0.06 [0.04-0.09] vs. mod V  + vehicle: 0.04 [0.03-0.09] µg/mg tissue, p > 0.99), sRAGE (mod V  + FG-3154: 1865 [1628-2252] vs. mod V  + vehicle: 1885 [1695-2159] pg/mL, p > 0.99) or histopathology. 'Double hit' VILI was characterized by inflammation, impaired oxygenation, pulmonary edema and histopathological lung injury. Blocking CTGF does not improve oxygenation nor reduce pulmonary edema in rats with VILI.
ArticleNumber 68
Author Ibelings, Roselique
van den Brom, Charissa E.
Polet, Chantal A.
Bozic, Caitlin
Roelofs, Joris J. T. H.
Juffermans, Nicole P.
Bongers, Annabel
Tuip-de Boer, Anita M.
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  organization: Department of Anesthesiology, Amsterdam UMC, VU University, Laboratory for Experimental Intensive Care and Anesthesiology (LEICA), Amsterdam UMC, University of Amsterdam, Department of Intensive Care Medicine, Amsterdam UMC, University of Amsterdam
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  givenname: Caitlin
  surname: Bozic
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  organization: Department of Anesthesiology, Amsterdam UMC, VU University, Laboratory for Experimental Intensive Care and Anesthesiology (LEICA), Amsterdam UMC, University of Amsterdam
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  givenname: Chantal A.
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  givenname: Joris J. T. H.
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  organization: Laboratory for Experimental Intensive Care and Anesthesiology (LEICA), Amsterdam UMC, University of Amsterdam, Department of Intensive Care Medicine, Amsterdam UMC, University of Amsterdam, OLVG Hospital
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CitedBy_id crossref_primary_10_1186_s12871_025_03251_3
crossref_primary_10_1016_j_jep_2025_120070
crossref_primary_10_3390_ijms26073000
Cites_doi 10.1001/jama.2016.0291
10.1371/journal.pbio.1000412
10.3389/fimmu.2022.896274
10.3389/fphys.2023.1253810
10.1097/MD.0000000000016531
10.1186/1755-1536-5-S1-S24
10.3390/jcm11061652
10.1186/1465-9921-10-19
10.1186/1755-1536-4-4
10.3892/mmr.2015.3537
10.1172/JCI0215849
10.1111/resp.14575
10.1016/S0140-6736(22)01485-4
10.1007/s00134-007-0651-x
10.1097/00000542-199805000-00022
10.3389/fphys.2018.00318
10.1186/s12931-023-02512-4
10.1016/S2213-2600(19)30262-0
10.1111/jcmm.12667
10.1186/s12964-021-00795-y
10.1203/PDR.0b013e318163a8cc
10.1152/ajplung.00055.2006
10.1093/jnci/djw339
10.1016/j.resp.2023.104142
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Issue 1
Keywords Edema
Ventilator-induced lung injury
Lung
ARDS
CTGF
Language English
License 2024. The Author(s).
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
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References C Kilkenny (829_CR10) 2010; 8
S Suzuki (829_CR19) 2022; 11
X Cui (829_CR7) 2018; 52
T Akter (829_CR1) 2022; 13
L Moraes (829_CR12) 2018; 9
K Nishina (829_CR13) 1998; 88
S Wu (829_CR22) 2008; 63
FG Eyal (829_CR8) 2007; 33
X Ran (829_CR14) 2023; 14
829_CR5
829_CR3
Z Yang (829_CR24) 2015; 12
Q Wang (829_CR21) 2011; 4
JA Frank (829_CR9) 2006; 291
JA Belperio (829_CR4) 2002; 110
Y Xie (829_CR23) 2019; 98
L Richeldi (829_CR15) 2020; 8
KE Lipson (829_CR11) 2012; 5
MJ Wallace (829_CR20) 2009; 10
LDJ Bos (829_CR6) 2022; 400
J Aoyama (829_CR2) 2023; 317
R Silasi-Mansat (829_CR17) 2015; 19
G Sgalla (829_CR16) 2023; 28
J Sun (829_CR18) 2023; 24
H Zhou (829_CR25) 2021; 19
References_xml – ident: 829_CR3
  doi: 10.1001/jama.2016.0291
– volume: 8
  year: 2010
  ident: 829_CR10
  publication-title: PLoS Biol
  doi: 10.1371/journal.pbio.1000412
– volume: 13
  year: 2022
  ident: 829_CR1
  publication-title: Front Immunol
  doi: 10.3389/fimmu.2022.896274
– volume: 14
  start-page: 1253810
  year: 2023
  ident: 829_CR14
  publication-title: Front Physiol
  doi: 10.3389/fphys.2023.1253810
– volume: 98
  year: 2019
  ident: 829_CR23
  publication-title: Medicine (baltimore)
  doi: 10.1097/MD.0000000000016531
– volume: 5
  start-page: S24
  issue: Suppl 1
  year: 2012
  ident: 829_CR11
  publication-title: Fibrogenesis Tissue Repair
  doi: 10.1186/1755-1536-5-S1-S24
– volume: 11
  start-page: 1652
  issue: 6
  year: 2022
  ident: 829_CR19
  publication-title: J Clin Med
  doi: 10.3390/jcm11061652
– volume: 10
  start-page: 19
  year: 2009
  ident: 829_CR20
  publication-title: Respir Res
  doi: 10.1186/1465-9921-10-19
– volume: 4
  start-page: 4
  year: 2011
  ident: 829_CR21
  publication-title: Fibrogenesis Tissue Repair
  doi: 10.1186/1755-1536-4-4
– volume: 12
  start-page: 1091
  issue: 1
  year: 2015
  ident: 829_CR24
  publication-title: Mol Med Rep
  doi: 10.3892/mmr.2015.3537
– volume: 110
  start-page: 1703
  issue: 11
  year: 2002
  ident: 829_CR4
  publication-title: J Clin Invest
  doi: 10.1172/JCI0215849
– volume: 28
  start-page: 954
  issue: 10
  year: 2023
  ident: 829_CR16
  publication-title: Respirology
  doi: 10.1111/resp.14575
– volume: 400
  start-page: 1145
  year: 2022
  ident: 829_CR6
  publication-title: Lancet
  doi: 10.1016/S0140-6736(22)01485-4
– volume: 33
  start-page: 1212
  year: 2007
  ident: 829_CR8
  publication-title: Intensive Care Med
  doi: 10.1007/s00134-007-0651-x
– volume: 88
  start-page: 1300
  issue: 5
  year: 1998
  ident: 829_CR13
  publication-title: Anesthesiology
  doi: 10.1097/00000542-199805000-00022
– volume: 9
  start-page: 318
  year: 2018
  ident: 829_CR12
  publication-title: Front Physiol
  doi: 10.3389/fphys.2018.00318
– volume: 52
  start-page: PA3666
  year: 2018
  ident: 829_CR7
  publication-title: Eur Resp J.
– volume: 24
  start-page: 227
  issue: 1
  year: 2023
  ident: 829_CR18
  publication-title: Respir Res
  doi: 10.1186/s12931-023-02512-4
– volume: 8
  start-page: 25
  year: 2020
  ident: 829_CR15
  publication-title: Lancet Respir Med
  doi: 10.1016/S2213-2600(19)30262-0
– volume: 19
  start-page: 2549
  issue: 11
  year: 2015
  ident: 829_CR17
  publication-title: J Cell Mol Med
  doi: 10.1111/jcmm.12667
– volume: 19
  start-page: 115
  year: 2021
  ident: 829_CR25
  publication-title: Cell Commun Signal
  doi: 10.1186/s12964-021-00795-y
– volume: 63
  start-page: 245
  year: 2008
  ident: 829_CR22
  publication-title: Pediatr Res
  doi: 10.1203/PDR.0b013e318163a8cc
– volume: 291
  start-page: L1191
  year: 2006
  ident: 829_CR9
  publication-title: Am J Physiol Lung Cell Mol Physiol
  doi: 10.1152/ajplung.00055.2006
– ident: 829_CR5
  doi: 10.1093/jnci/djw339
– volume: 317
  year: 2023
  ident: 829_CR2
  publication-title: Respir Physiol Neurobiol
  doi: 10.1016/j.resp.2023.104142
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Snippet Background Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can...
Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can augment lung...
BackgroundAcute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation can...
Abstract Background Acute respiratory distress syndrome (ARDS) is characterized by alveolar edema that can progress to septal fibrosis. Mechanical ventilation...
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SubjectTerms Animals
Antibodies
Antibodies, Neutralizing - pharmacology
ARDS
Biomedical and Life Sciences
Biomedicine
Blood gas analysis
Blood pressure
Carotid arteries
Catheters
Connective tissue
Connective Tissue Growth Factor - antagonists & inhibitors
Connective Tissue Growth Factor - metabolism
CTGF
Disease Models, Animal
Edema
Growth factors
Ketamine
Lung
Lung - metabolism
Lung - pathology
Lungs
Male
Molecular Medicine
Permeability
Pulmonary Edema - etiology
Pulmonary Edema - metabolism
Pulmonary fibrosis
Rats
Rats, Sprague-Dawley
Receptor for Advanced Glycation End Products - antagonists & inhibitors
Receptor for Advanced Glycation End Products - metabolism
Research Article
Ventilator-induced lung injury
Ventilator-Induced Lung Injury - drug therapy
Ventilator-Induced Lung Injury - metabolism
Ventilator-Induced Lung Injury - pathology
Ventilators
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Title Effect of antibody-mediated connective tissue growth factor neutralization on lung edema in ventilator-induced lung injury in rats
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