ArticleRespiratory research2019
Reverse-D-4F improves endothelial progenitor cell function and attenuates LPS-induced acute lung injury.
Article in Respiratory research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- The Role and Mechanism of Endothelial Progenitor Cell-Derived Extracellular Vesicles in Vascular Repair of Ischemic Heart Disease.Journal of cardiovascular translational research · 2026Review
- ApoA1/HDL and sepsis-associated vascular endothelial injury: a narrative review.Critical care (London, England) · 2025Review
- From copper homeostasis to cuproptosis: a new perspective on CNS immune regulation and neurodegenerative diseases.Frontiers in neurology · 2025Review
- Unraveling the deadly dance: endothelial cells and neutrophils in sepsis-induced acute lung injury/acute respiratory distress syndrome.Frontiers in cell and developmental biology · 2025Review
- Synthetic Amphipathic Helical Peptide L-37pA Ameliorates the Development of Acute Respiratory Distress Syndrome (ARDS) and ARDS-Induced Pulmonary Fibrosis in Mice.International journal of molecular sciences · 2024Article
- Anthrahydroquinone‑2,6‑disulfonate attenuates PQ‑induced acute lung injury through decreasing pulmonary microvascular permeability via inhibition of the PI3K/AKT/eNOS pathway.International journal of molecular medicine · 2024Article
- A Current Update on the Role of HDL-Based Nanomedicine in Targeting Macrophages in Cardiovascular Disease.Pharmaceutics · 2023Review
- Inhibiting P2Y12 receptor relieves LPS-induced inflammation and endothelial dysfunction.Immunity, inflammation and disease · 2022Article
- HDL and Therapy.Advances in experimental medicine and biology · 2022Article
- Hydrogen Repairs LPS-Induced Endothelial Progenitor Cells InjuryFrontiers in pharmacology · 2022Article
- Post-Stroke Administration of L-4F Promotes Neurovascular and White Matter Remodeling in Type-2 Diabetic Stroke Mice.Frontiers in neurology · 2022Article
- Apolipoprotein-AI and AIBP synergetic anti-inflammation as vascular diseases therapy: the new perspective.Molecular and cellular biochemistry · 2021Review
- Endothelial progenitor cells as critical mediators of environmental air pollution-induced cardiovascular toxicity.American journal of physiology. Heart and circulatory physiology · 2021Review
- Review
- Cigarette smoke extract affects methylation status and attenuates Sca-1 expression of mouse endothelial progenitor cell in vitro.Tobacco induced diseases · 2021Article
- Vagal α7nAChR signaling regulates α7nAChRStem cell research & therapy · 2020Article
- Madecassoside Protects Against LPS-Induced Acute Lung InjuryFrontiers in pharmacology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundPatients with acute lung injury (ALI) have increased levels of pro-inflammatory mediators, which impair endothelial progenitor cell (EPC) function. Increasing the number of EPC and alleviating EPC dysfunction induced by pro-inflammatory mediators play important roles in suppressing ALI development. Because the high density lipoprotein reverse-D-4F (Rev-D4F) improves EPC function, we hypothesized that it might repair lipopolysaccharide (LPS)-induced lung damage by improving EPC numbers and function in an LPS-induced ALI mouse model.
methodsLPS was used to induce ALI in mice, and then the mice received intraperitoneal injections of Rev-D4F. Immunohistochemical staining, flow cytometry, MTT, transwell, and western blotting were used to assess the effect of Rev-D4F on repairment of lung impairment, and improvement of EPC numbers and function, as well as the signaling pathways involved.
resultsRev-D4F inhibits LPS-induced pulmonary edema and decreases plasma levels of the pro-inflammatory mediators TNF-α and ET-1 in ALI mice. Rev-D4F inhibited infiltration of red and white blood cells into the interstitial space, reduced lung injury-induced inflammation, and restored injured pulmonary capillary endothelial cells. In addition, Rev-D4F increased numbers of circulating EPC, stimulated EPC differentiation, and improved EPC function impaired by LPS. Rev-D4F also acted via a PI3-kinase-dependent mechanism to restore levels of phospho-AKT, eNOS, and phospho-eNOS suppressed by LPS.
conclusionsThese findings indicate that Rev-D4F has an important vasculoprotective role in ALI by improving the EPC numbers and functions, and Rev-D4F reverses LPS-induced EPC dysfuncion partially through PI3K/AKT/eNOS signaling pathway.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.