scispace - formally typeset
F

Friedrich Grimminger

Researcher at University of Giessen

Publications -  431
Citations -  33019

Friedrich Grimminger is an academic researcher from University of Giessen. The author has contributed to research in topics: Pulmonary hypertension & Hypoxia (medical). The author has an hindex of 83, co-authored 402 publications receiving 30002 citations. Previous affiliations of Friedrich Grimminger include Goethe University Frankfurt.

Papers
More filters
Journal ArticleDOI

Hypoxic Pulmonary Hypertension in Mice with Constitutively Active Platelet-Derived Growth Factor Receptor-β:

TL;DR: Findings substantiate the major role of PDGFR activation in pulmonary vascular remodeling by a genetic approach and suggest a role for SDF-1α/CXCR4 axis in pulmonaryascular remodeling and point to a potential interaction between the chemokine SDF -1 and the growth factor PDGF signaling.
Journal ArticleDOI

Role of Actin Depolymerization in the Surfactant Secretory Response of Alveolar Epithelial Type II Cells

TL;DR: Data suggest that the state of actin polymerization is intimately linked to the exocytosis process underlying surfactant secretion in AET2, and microfilament system-related compartmentalization effects and/or or the impact of the stateof actin assembly on signaling events may be considered as underlying events.
Journal ArticleDOI

Therapeutic efficacy of azaindole-1 in experimental pulmonary hypertension

TL;DR: Azaindole-1 provided therapeutic benefit in experimental PH, and this may be attributable to its potent vasorelaxant and antiproliferative effects and may offer a useful approach for treatment of PH.
Journal ArticleDOI

Endotoxin induces proliferation of NSCLC in vitro and in vivo: role of COX-2 and EGFR activation.

TL;DR: Investigation of the effect of bacterial lipopolysaccharides on tumor proliferation in vitro in the non-small cell lung cancer cell line A549 revealed that the proliferative effect of LPS was dependent on CD14 and Toll-like receptor (TLR)4 and blocking of the epidermal growth factor receptor (EGFR) also decreased LPS-induced proliferation of A549 cells.