ArticleProceedings of the National Academy of Sciences of the United States of America2013
Identification of apolipoprotein D as a cardioprotective gene using a mouse model of lethal atherosclerotic coronary artery disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- The Lipocalin Apolipoprotein D Functional Portrait: A Systematic Review.Frontiers in physiology · 2021Pooled it
- GOT2-mediated suppression of CoQCommunications biology · 2026Article
- Senescence-related epicardial adipocyte genes lead to immune infiltration and myocardial infarction progression.Frontiers in cardiovascular medicine · 2026Article
- HVJ-E links Apolipoprotein d to antitumor effects.Journal for immunotherapy of cancer · 2025Article
- Plasma apolipoprotein concentrations and occurrence of cardiovascular events in the general population: an exploratory analysis.Atherosclerosis plus · 2025Article
- Article
- Stromal cell-derived factor-1 alpha improves cardiac function in a novel diet-induced coronary atherosclerosis model, the SR-B1ΔCT/LDLR KO mouse.Atherosclerosis · 2024Article
- Plasma Proteomics-Based Discovery of Mechanistic Biomarkers of Hyperbaric Stress and Pulmonary Oxygen Toxicity.Metabolites · 2023Article
- MAVS signaling is required for preventing persistent chikungunya heart infection and chronic vascular tissue inflammation.Nature communications · 2023Article
- Remodeled eX vivo muscle engineered tissue improves heart function after chronic myocardial ischemia.Scientific reports · 2023Article
- Apolipoprotein D in Oxidative Stress and Inflammation.Antioxidants (Basel, Switzerland) · 2023Review
- Lipocalin family proteins and their diverse roles in cardiovascular disease.Pharmacology & therapeutics · 2023Review
- The Neuroprotective Lipocalin Apolipoprotein D Stably Interacts with Specific Subtypes of Detergent-Resistant Membrane Domains in a Basigin-Independent Manner.Molecular neurobiology · 2022Article
- Premature Myocardial Infarction: A Rising Threat.Balkan medical journal · 2022Review
- Multi-omic Analysis of Non-human Primate Heart after Partial-body Radiation with Minimal Bone Marrow Sparing.Health physics · 2021Article
- RNA-Seq reveals changes in human placental metabolism, transport and endocrinology across the first-second trimester transition.Biology open · 2021Article
- Genome-wide transcriptome study using deep RNA sequencing for myocardial infarction and coronary artery calcification.BMC medical genomics · 2021Article
- Studies of ApoDCellular and molecular life sciences : CMLS · 2021Article
- Article
- Human cardiac progenitor cell activation and regeneration mechanisms: exploring a novel myocardial ischemia/reperfusion in vitro model.Stem cell research & therapy · 2019Article
Corrections and comments
- Commented on by
Authors and funding
13 authors at 7 institutions in 1 country.
Funding
Abstract
Mice with homozygous null mutations in the HDL receptor (scavenger receptor class B, type I, or SR-BI) and apolipoprotein E (apoE) genes [SR-BI/apoE double KO (SR-BI(-/-)/apoE(-/-) or dKO) mice] spontaneously develop occlusive, atherosclerotic coronary artery disease (CAD) and die prematurely (50% mortality at 42 d of age). Using microarray mRNA expression profiling, we identified genes whose expression in the hearts of dKO mice changed substantially during disease progression [at 21 d of age (no CAD), 31 d of age (small myocardial infarctions), and 43 d of age (extensive myocardial infarctions) vs. CAD-free SR-BI(+/-)/apoE(-/-) controls]. Expression of most genes that increased >sixfold in dKO hearts at 43 d also increased after coronary artery ligation. We examined the influence and potential mechanism of action of apolipoprotein D (apoD) whose expression in dKO hearts increased 80-fold by 43 d. Analysis of ischemia/reperfusion-induced myocardial infarction in both apoD KO mice and wild-type mice with abnormally high plasma levels of apoD (adenovirus-mediated hepatic overexpression) established that apoD reduces myocardial infarction. There was a correlation of apoD's ability to protect primary cultured rat cardiomyocytes from hypoxia/reoxygenation injury with its potent ability to inhibit oxidation in a standard antioxidation assay in vitro. We conclude that dKO mice represent a useful mouse model of CAD and apoD may be part of an intrinsic cardioprotective system, possibly as a consequence of its antioxidation activity.
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.