Glycosylphosphatidylinositol-induced cardiac myocyte death might contribute to the fatal outcome of Plasmodium falciparum malaria

Wennicke, Kathrin; Debierre‐Grockiego, Françoise; Wichmann, Dominic; Brattig, Norbert W.; Pankuweit, Sabine; Maisch, Bernhard; Schwarz, Ralph Τ.; Ruppert, Volker

doi:10.1007/s10495-008-0217-6

Cited by 25 publications

(18 citation statements)

References 24 publications

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“…By analyzing gene expression of cardiomyocytes treated with purified P. falciparum glycosyl phosphatidylinositol (GPI), which act as a toxin in the malaria pathogenesis, up-regulated genes related to apoptosis and myocardial damages were found, indicating that P. falciparum GPI can also induce cardiomyocyte apoptosis [37]. In the same study, a falciparum infected patient presented with heart failure with typical signs of cardiac myocyte apoptosis, suggesting that his complications could have been caused by the presence of this toxin.…”

Section: Effects Of Malaria On Cardiac Musclementioning

confidence: 99%

The effect of malaria and anti-malarial drugs on skeletal and cardiac muscles

Marrelli

Brotto

2016

Malar J

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Malaria remains one of the most important infectious diseases in the world, being a significant public health problem associated with poverty and it is one of the main obstacles to the economy of an endemic country. Among the several complications, the effects of malaria seem to target the skeletal muscle system, leading to symptoms, such as muscle aches, muscle contractures, muscle fatigue, muscle pain, and muscle weakness. Malaria cause also parasitic coronary artery occlusion. This article reviews the current knowledge regarding the effect of malaria disease and the anti-malarial drugs on skeletal and cardiac muscles. Research articles and case report publications that addressed aspects that are important for understanding the involvement of malaria parasites and anti-malarial therapies affecting skeletal and cardiac muscles were analysed and their findings summarized. Sequestration of red blood cells, increased levels of serum creatine kinase and reduced muscle content of essential contractile proteins are some of the potential biomarkers of the damage levels of skeletal and cardiac muscles. These biomarkers might be useful for prevention of complications and determining the effectiveness of interventions designed to protect cardiac and skeletal muscles from malaria-induced damage.

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Section: Effects Of Malaria On Cardiac Musclementioning

confidence: 99%

The effect of malaria and anti-malarial drugs on skeletal and cardiac muscles

Marrelli

Brotto

2016

Malar J

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“…A diversity of antigens produced by pathogenic bacteria such as enterotoxins, hemolysins, lethal toxins, lipotechoic acid, and lipopolysaccharide, have the ability to promote apoptosis in several types of host cells including T and B lymphocytes, dendritic cells, monocytes, macrophages, neutrophils, endothelial cells, epithelial cells (Ulett and Adderson, 2006; Carrero and Unanue, 2012). Similarly, malaria toxins glycosylphosphatidylinositol and hemozoin purified from P. falciparum showed proapoptotic activity in cardiomyocytes and erythroblasts, respectively (Wennicke et al, 2008; Lamikanra et al, 2009). Moreover, such apoptogenic effect of parasite factors was recorded by incubating brain vascular endothelial and neuroglia cells with P. falciparum -pRBC conditioned medium (Wilson et al, 2008), and induction of apoptosis in lung endothelial cells can additionally take place by physical contact due to pRBC adhesion phenomenon (Pino et al, 2003).…”

Section: Malaria and Erythrocytic Apoptosis Inducersmentioning

confidence: 99%

Evidencing the Role of Erythrocytic Apoptosis in Malarial Anemia

Totino

Daniel-Ribeiro

Ferreira-da-Cruz

2016

Front. Cell. Infect. Microbiol.

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In the last decade it has become clear that, similarly to nucleated cells, enucleated red blood cells (RBCs) are susceptible to programmed apoptotic cell death. Erythrocytic apoptosis seems to play a role in physiological clearance of aged RBCs, but it may also be implicated in anemia of different etiological sources including drug therapy and infectious diseases. In malaria, severe anemia is a common complication leading to death of children and pregnant women living in malaria-endemic regions of Africa. The pathogenesis of malarial anemia is multifactorial and involves both ineffective production of RBCs by the bone marrow and premature elimination of non-parasitized RBCs, phenomena potentially associated with apoptosis. In the present overview, we discuss evidences associating erythrocytic apoptosis with the pathogenesis of severe malarial anemia, as well as with regulation of parasite clearance in malaria. Efforts to understand the role of erythrocytic apoptosis in malarial anemia can help to identify potential targets for therapeutic intervention based on apoptotic pathways and consequently, mitigate the harmful impact of malaria in global public health.

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“…GPI-treated cardiomyocytes exhibit a down-regulation of the Bcl-2 gene [98]. Moreover, calcitriol inhibits hepatocyte apoptosis in rat allografts by regulating apoptosisassociated genes and increasing Bcl-2 levels [99].…”

Section: The Genomic Factors Associated With Vitamin D In Malariamentioning

confidence: 99%

The role of Vitamin D in malaria

Lương

Nguyễn

2015

J Infect Dev Ctries

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An abnormal calcium-parathyroid hormone (PTH)-vitamin D axis has been reported in patients with malaria infection. A role for vitamin D in malaria has been suggested by many studies. Genetic studies have identified numerous factors that link vitamin D to malaria, including human leukocyte antigen genes, toll-like receptors, heme oxygenase-1, angiopoietin-2, cytotoxic T lymphocyte antigen-4, nucleotide-binding oligomerization domain-like receptors, and Bcl-2. Vitamin D has also been implicated in malaria via its effects on the Bacillus CalmetteGuerin (BCG) vaccine, matrix metalloproteinases, mitogen-activated protein kinase pathways, prostaglandins, reactive oxidative species, and nitric oxide synthase. Vitamin D may be important in malaria; therefore, additional research on its role in malaria is needed.

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Glycosylphosphatidylinositol-induced cardiac myocyte death might contribute to the fatal outcome of Plasmodium falciparum malaria

Abstract: Plasmodium falciparum GPI-induced apoptosis might participate in the lethality of malaria.

Cited by 25 publications

References 24 publications

The effect of malaria and anti-malarial drugs on skeletal and cardiac muscles

The effect of malaria and anti-malarial drugs on skeletal and cardiac muscles

Evidencing the Role of Erythrocytic Apoptosis in Malarial Anemia

The role of Vitamin D in malaria

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