Placental malaria and preeclampsia: shared pathways and translational perspectives in endemic regions.
6 affiliations
- 1Department of Anatomy, College of Health Sciences, University of Ghana Medical School, University of Ghana, Accra, Ghana.
- 2Department of Immunology, College of Health Science, Noguchi Memorial Institute for Medical Research, University of Ghana, Accra, Ghana.
- 3Department of Neurological Surgery, Keck Medicine of USC, University of Southern California, Los Angeles, CA, 90033, USA.
- 4Alfred E. Mann Department of Biomedical Engineering, Viterbi School of Engineering, University of Southern California, Los Angeles, CA, 90089, USA.
- 5Department of Animal Biology and Conservation Science, College of Basic and Applied Science, University of Ghana, Accra, Ghana.
- 6Department of Immunology, College of Health Science, Noguchi Memorial Institute for Medical Research, University of Ghana, Accra, Ghana. [email protected].
Abstract
Placental malaria (PM), driven by sequestration of Plasmodium falciparum-infected erythrocytes within the placental intervillous space, remains a major contributor to adverse maternal and fetal outcomes in endemic regions. Increasing evidence suggests that PM may also contribute to the development of preeclampsia (PE), a leading cause of maternal and perinatal morbidity and mortality worldwide. Although PM and PE arise from distinct initiating events, Plasmodium falciparum sequestration in PM and defective spiral artery remodeling in PE, both conditions converge on shared placental and systemic biological pathways. In PM, P. falciparum-infected red blood cells (iRBCs) sequester within the placental intervillous space through binding of parasite-expressed variant surface antigen 2-chondroitin sulfate A (VAR2CSA) adhesion to chondroitin sulfate A (CSA) on the syncytiotrophoblast. This sequestration, together with the accumulation of parasite derived products such as hemozoin, promotes local inflammation, syncytiotrophoblast stress, and disruption of placental vascular homeostasis. In PE, placental hypoperfusion and ischemia-reperfusion injury induce oxidative stress and abnormal trophoblast turnover. Despite these different origins, both conditions produce some overlapping patterns of placental injury including angiogenic dysregulation, characterized by elevated anti-angiogenic factors and reduced pro-angiogenic mediators. This convergence is further marked by activation of inflammatory signalling through NF-κB and inflammasome pathways, oxidative injury, complement activation, and systemic endothelial dysfunction. This review synthesizes current evidence on the shared biological pathways linking PM and PE and explores how malaria-induced placental injury may increase susceptibility to PE. We also examine the implications of overlapping biomarker signatures for diagnosis and risk stratification in malaria-endemic settings. Key knowledge gaps are highlighted, and priorities for future research are proposed to inform integrated strategies for malaria control and improved clinical management of PE in malaria-endemic settings.
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BibTeX
@article{quaye2026placental,
title = {{Placental malaria and preeclampsia: shared pathways and translational perspectives in endemic regions.}},
author = {Dorcas Quaye and Enoch Acheampong Konadu and Timothy Elorm Letsa and Philip Asante and Samuel Amponsah-Effah and Daniel Oduro and Dorotheah Obiri},
journal = {Malaria journal},
year = {2026},
month = jul,
doi = {10.1186/s12936-026-06071-z},
url = {https://europepmc.org/article/MED/42958321},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Placental malaria and preeclampsia: shared pathways and translational perspectives in endemic regions.
AU - Dorcas Quaye
AU - Enoch Acheampong Konadu
AU - Timothy Elorm Letsa
AU - Philip Asante
AU - Samuel Amponsah-Effah
AU - Daniel Oduro
AU - Dorotheah Obiri
PY - 2026
DA - 2026/07/31
JO - Malaria journal
DO - 10.1186/s12936-026-06071-z
UR - https://europepmc.org/article/MED/42958321
AB - Placental malaria (PM), driven by sequestration of Plasmodium falciparum-infected erythrocytes within the placental intervillous space, remains a major contributor to adverse maternal and fetal outcomes in endemic regions. Increasing evidence suggests that PM may also contribute to the development of preeclampsia (PE), a leading cause of maternal and perinatal morbidity and mortality worldwide. Although PM and PE arise from distinct initiating events, Plasmodium falciparum sequestration in PM and defective spiral artery remodeling in PE, both conditions converge on shared placental and systemic biological pathways. In PM, P. falciparum-infected red blood cells (iRBCs) sequester within the placental intervillous space through binding of parasite-expressed variant surface antigen 2-chondroitin sulfate A (VAR2CSA) adhesion to chondroitin sulfate A (CSA) on the syncytiotrophoblast. This sequestration, together with the accumulation of parasite derived products such as hemozoin, promotes local inflammation, syncytiotrophoblast stress, and disruption of placental vascular homeostasis. In PE, placental hypoperfusion and ischemia-reperfusion injury induce oxidative stress and abnormal trophoblast turnover. Despite these different origins, both conditions produce some overlapping patterns of placental injury including angiogenic dysregulation, characterized by elevated anti-angiogenic factors and reduced pro-angiogenic mediators. This convergence is further marked by activation of inflammatory signalling through NF-κB and inflammasome pathways, oxidative injury, complement activation, and systemic endothelial dysfunction. This review synthesizes current evidence on the shared biological pathways linking PM and PE and explores how malaria-induced placental injury may increase susceptibility to PE. We also examine the implications of overlapping biomarker signatures for diagnosis and risk stratification in malaria-endemic settings. Key knowledge gaps are highlighted, and priorities for future research are proposed to inform integrated strategies for malaria control and improved clinical management of PE in malaria-endemic settings.
SN - 1475-2875
ER -