ArticleLife sciences2012
The novel ETA receptor antagonist HJP-272 prevents cerebral microvascular hemorrhage in cerebral malaria and synergistically improves survival in combination with an artemisinin derivative.
Article in Life sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Polycyclitol Derivatives Restore Long- Term Memory Via cdk5/p25 Activation of Tau Signaling in Experimental Cerebral Malaria.Neurochemical research · 2025Article
- Cerebral Malaria and Neuronal Implications of Plasmodium Falciparum Infection: From Mechanisms to Advanced Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Review
- Pathophysiology and neurologic sequelae of cerebral malaria.Malaria journal · 2020Review
- Endothelins in inflammatory neurological diseases.Pharmacology & therapeutics · 2019Review
- Neuroinflammation and Infection: Molecular Mechanisms Associated with Dysfunction of Neurovascular Unit.Frontiers in cellular and infection microbiology · 2017Review
- Local mild hypothermia therapy as an augmentation strategy for minimally invasive surgery of hypertensive intracerebral hemorrhage: a meta-analysis of randomized clinical trials.Neuropsychiatric disease and treatment · 2017Article
- Endothelin-1 Treatment Induces an Experimental Cerebral Malaria-Like Syndrome in C57BL/6 Mice Infected with Plasmodium berghei NK65.The American journal of pathology · 2016Article
- Endothelin-1 Mediates Brain Microvascular Dysfunction Leading to Long-Term Cognitive Impairment in a Model of Experimental Cerebral Malaria.PLoS pathogens · 2016Article
- Pathogenesis of cerebral malaria: new diagnostic tools, biomarkers, and therapeutic approaches.Frontiers in cellular and infection microbiology · 2015Review
- Experimental cerebral malaria pathogenesis--hemodynamics at the blood brain barrier.PLoS pathogens · 2014Article
- Endothelin-1 and its role in the pathogenesis of infectious diseases.Life sciences · 2014Review
- Vascular dysfunction as a target for adjuvant therapy in cerebral malaria.Memorias do Instituto Oswaldo Cruz · 2014Review
- Role of the aryl hydrocarbon receptor in the immune response profile and development of pathology during Plasmodium berghei Anka infection.Infection and immunity · 2014Article
- Fatal cerebral malaria: a venous efflux problem.Frontiers in cellular and infection microbiology · 2014Review
- Potential efficacy of citicoline as adjunct therapy in treatment of cerebral malaria.Antimicrobial agents and chemotherapy · 2014Article
- A new hypothesis on the manifestation of cerebral malaria: the secret is in the liver.Medical hypotheses · 2013Article
- Cerebral malaria: we have come a long way.The American journal of pathology · 2012Review
- The Einstein-Brazil Fogarty: A decade of synergy.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology]Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
aimTo investigate the association between vasculopathy and survival during experimental cerebral malaria (ECM), and to determine whether targeting the endothelin-1 (ET-1) pathway alone or in combination with the anti-malaria drug artemether (a semi-synthetic derivative of artemisinin) will improve microvascular hemorrhage and survival. MAIN
methodsC57BL/6 mice infected with Plasmodium berghei ANKA (PbA) were randomly assigned to four groups: no treatment, artemether treated, ET(A) receptor antagonist (HJP-272) treated, or HJP-272 and artemether treated. The uninfected control mice were treated with HJP-272 and artemether. We analyzed survival, cerebral hemorrhage, weight change, blood glucose levels and parasitemia. KEY
findingsOur studies demonstrated decreased brain hemorrhage in PbA-infected (ECM) mice treated when HJP-272, a 1,3,6-trisubstituted-2-carboxy-quinol-4-one novel ET(A) receptor antagonist synthesized by our group, is used in conjunction with artemether, an anti-malarial agent. In addition, despite adversely affecting parasitemia and weight in non-artemether treated infected mice, HJP-272, seemed to confer some survival benefit when used as adjunctive therapy, though this did not reach significance. SIGNIFICANCE: Previous studies demonstrate that the endothelin pathway is associated with vasculopathy, neuronal injury and inflammation in ECM. As demonstrated here, components of the ET-1 pathway may be important targets for adjunctive therapy in ECM, and may help in preventing hemorrhage and in improving survival when used as adjunctive therapy during malaria infection. The data presented suggest that our novel agent, HJP-272, may ameliorate alterations in the vasculature which can potentially lead to inflammation, neurological dysfunction, and subsequent death in mice with ECM.
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