Our study reveals the potential of precision-cut lung slices as an platform to study the growth/survival of spp. that can facilitate the development of new anti-fungal drugs.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10790776 | PMC |
| http://dx.doi.org/10.1128/mbio.01464-23 | DOI Listing |
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Monash University, Department of Pharmacology, Biomedicine Discovery Institute, Clayton, Victoria, Australia.
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View Article and Find Full Text PDFDextromethorphan inhibits collagen and collagen-like cargo secretion to ameliorate lung fibrosis.
Sci Transl Med
December 2024
Cell Biology and Biophysics Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany.
Excessive deposition of fibrillar collagen in the interstitial extracellular matrix (ECM) of human lung tissue causes fibrosis, which can ultimately lead to organ failure. Despite our understanding of the molecular mechanisms underlying the disease, no cure for pulmonary fibrosis has yet been found. We screened a drug library and found that dextromethorphan (DXM), a cough expectorant, reduced the amount of excess fibrillar collagen deposited in the ECM in cultured primary human lung fibroblasts, a bleomycin mouse model, and a cultured human precision-cut lung slice model of lung fibrosis.
View Article and Find Full Text PDFPrecision cut lung slices: an innovative tool for lung transplant research.
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Department of Surgery, University of Florida, Gainesville, FL, United States.
Lung ischemia-reperfusion injury (IRI), a common complication after lung transplantation (LTx), plays a crucial role in both primary graft dysfunction (PGD) and chronic lung allograft dysfunction (CLAD) thereby adversely impacting the clinical outcomes in these patient cohorts. Lung IRI is characterized by several molecular events including immune cell infiltration, reactive oxygen species (ROS) generation, calcium overload, inflammation and various forms of cell death pathways. Currently, no therapeutic agents are available to clinically prevent lung IRI.
View Article and Find Full Text PDFATP citrate lyase drives vascular remodeling in systemic and pulmonary vascular diseases through metabolic and epigenetic changes.
Sci Transl Med
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Pulmonary Hypertension Research Group, Québec Heart and Lung Institute Research Centre, Québec City, QC G1V 4G5, Canada.
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View Article and Find Full Text PDFLeukemia inhibitory factor (LIF) receptor amplifies pathogenic activation of fibroblasts in lung fibrosis.
Proc Natl Acad Sci U S A
December 2024
Department of Medicine, Division of Rheumatology, Inflammation and Immunity, Brigham and Women's Hospital, Boston, MA 02115.
Article Synopsis
- Fibrosis contributes to serious damage in organs, but treatments targeting specific activators have often failed, leading researchers to focus on the leukemia inhibitory factor receptor (LIFR) as a key player in fibrotic diseases like idiopathic pulmonary fibrosis (IPF).
- In IPF, myofibroblasts highly express LIF, and fibroblasts in key fibrotic areas coexpress LIF and LIFR, demonstrating LIFR's role in amplifying signals from other fibrotic drivers like TGFβ1, IL-4, and IL-13.
- Blocking LIFR reduces the activation of profibrotic genes and highlights LIFR's function as a master amplifier of harmful signals
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