ReviewCurrent pharmaceutical design2012
CD36 as a therapeutic target for endothelial dysfunction in stroke.
Review in Current pharmaceutical design, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 51 citations in OpenAlex.
- Transcriptomic insights into the co-occurring psychological symptoms and cardiovascular risks among military service members and veterans with mild traumatic brain injury: A LIMBIC-CENC study.Brain, behavior, & immunity - health · 2026Article
- Endothelial GATAD1 Exacerbates Blood-brain Barrier Dysfunction in Ischemic Stroke through Caveolae-mediated Transcytosis.Neuroscience bulletin · 2026Article
- Targeting the Jun-Irf8-CD36 axis attenuates fibrotic scar formation and promotes functional recovery after spinal cord injury.Burns & trauma · 2026Article
- Activation of endothelial TRPM2 exacerbates blood-brain barrier degradation in ischemic stroke.Cardiovascular research · 2024Article
- Role of CD36 in central nervous system diseases.Neural regeneration research · 2024Review
- Article
- NWorld journal of diabetes · 2023Article
- A Metabolic Signature to Monitor Endothelial Cell Differentiation, Activation, and Vascular Organization.Biomedicines · 2022Article
- TRPM2 deficiency in mice protects against atherosclerosis by inhibiting TRPM2-CD36 inflammatory axis in macrophages.Nature cardiovascular research · 2022Article
- Diversity of Lipid Function in Atherogenesis: A Focus on Endothelial Mechanobiology.International journal of molecular sciences · 2021Review
- CD36 promotes vasculogenic mimicry in melanoma by mediating adhesion to the extracellular matrix.BMC cancer · 2021Article
- Organelle Crosstalk Regulators Are Regulated in Diseases, Tumors, and Regulatory T Cells: Novel Classification of Organelle Crosstalk Regulators.Frontiers in cardiovascular medicine · 2021Article
- Review
- Endothelial Cells (ECs) Metabolism: A Valuable Piece to Disentangle Cancer Biology.Advances in experimental medicine and biology · 2020Review
- Blood-Related Toxicity after Traumatic Brain Injury: Potential Targets for Neuroprotection.Molecular neurobiology · 2020Review
- Endothelial Progenitor Cells Modulate Inflammation-Associated Stroke Vasculome.Stem cell reviews and reports · 2019Article
- Maoberry (Antidesma bunius) ameliorates oxidative stress and inflammation in cardiac tissues of rats fed a high-fat diet.BMC complementary and alternative medicine · 2018Article
- The Contribution of Autoantibodies to Inflammatory Cardiovascular Pathology.Frontiers in immunology · 2018Review
- Exposure to traffic-generated air pollutants mediates alterations in brain microvascular integrity in wildtype mice on a high-fat diet.Environmental research · 2018Article
- Sulfosuccinimidyl oleate sodium is neuroprotective and alleviates stroke-induced neuroinflammation.Journal of neuroinflammation · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Stroke pathology involves multifactorial pro-death responses, including inflammation, oxidative stress, vascular dysfunction, and activation of necrotic and apoptotic pathways. The interruption of a single specific pathway in defined stroke model systems has not been sufficient to address the multifactorial nature of stroke-induced injuries in the human population. CD36 is a class B scavenger receptor that functions in regulating normal physiological and pathological functions. CD36 pathways are activated by several distinct ligands. Convergence of these pathways results in inflammatory responses and endothelial dysfunction, which may be an underlying cause of cardio- and cerebrovascular diseases. The current review describes receptor CD36-ligand interactions relevant to endothelial function and discusses how targeting CD36 may have therapeutic utility in stroke.
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.