ArticleArteriosclerosis, thrombosis, and vascular biology2018
Impaired Collateral Vessel Formation in Sickle Cell Disease.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Characterizing pregnancy outcomes in a humanized mouse model of sickle cell disease.British journal of haematology · 2025Article
- Angiogenic and inflammatory responses in human induced microglia-like (iMG) cells from patients with Moyamoya disease.Scientific reports · 2023Article
- Intestinal barrier dysfunction in murine sickle cell disease is associated with small intestine neutrophilic inflammation, oxidative stress, and dysbiosis.FASEB bioAdvances · 2023Article
- Impaired post-stroke collateral circulation in sickle cell anemia mice.Frontiers in neurology · 2023Article
- Increasing nitric oxide bioavailability fails to improve collateral vessel formation in humanized sickle cell mice.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- RASAL3 Is a Putative RasGAP Modulating Inflammatory Response by Neutrophils.Frontiers in immunology · 2021Article
- Annual Report on Sex in Preclinical Studies:Arteriosclerosis, thrombosis, and vascular biology · 2020Review
- Red blood cells modulate structure and dynamics of venous clot formation in sickle cell disease.Blood · 2019Article
- Investigating the potential of the secretome of mesenchymal stem cells derived from sickle cell disease patients.PloS one · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveThe adaptive response to vascular injury is the formation of functional collateral vessels to maintain organ integrity. Many of the clinical complications associated with sickle cell disease can be attributed to repeated bouts of vascular insufficiency, yet the detailed mechanisms of collateral vessel formation after injury are largely unknown in sickle cell disease. Here, we characterize postischemic neovascularization in sickle cell disease and the role of neutrophils in the production of reactive oxygen species. APPROACH AND
resultsWe induced hindlimb ischemia by ligation of the femoral artery in Townes SS (sickle cell) mice compared with AA (wild type) mice. Perfusion recovery, ascertained using LASER (light amplification by stimulated emission of radiation) Doppler perfusion imaging, showed significant diminution in collateral vessel formation in SS mice after hindlimb ischemia (76±13% AA versus 34±10% in SS by day 28;
conclusionsOur data suggest dysfunctional collateral vessel formation in SS mice after vascular injury and provide a mechanistic basis for the multiple vascular complications of sickle cell disease.
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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.