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Article ; Online: The Concept of Thromboinflammation.

Schrottmaier, Waltraud C / Assinger, Alice

2024 Volume 44, Issue 1, Page(s) 21–30

Abstract: Inflammation and thrombosis are intricate and closely interconnected biological processes that are not yet fully understood and lack effective targeted therapeutic approaches. Thrombosis initiated by inflammatory responses, known as immunothrombosis, can ...

Abstract	Inflammation and thrombosis are intricate and closely interconnected biological processes that are not yet fully understood and lack effective targeted therapeutic approaches. Thrombosis initiated by inflammatory responses, known as immunothrombosis, can confer advantages to the host by constraining the spread of pathogens within the bloodstream. Conversely, platelets and the coagulation cascade can influence inflammatory responses through interactions with immune cells, endothelium, or complement system. These interactions can lead to a state of heightened inflammation resulting from thrombotic processes, termed as thromboinflammation. This review aims to comprehensively summarize the existing knowledge of thromboinflammation and addressing its significance as a challenging clinical issue.
MeSH term(s)	Humans ; Thrombosis ; Inflammation ; Thromboinflammation ; Blood Coagulation ; Blood Platelets
Language	English
Publishing date	2024-02-28
Publishing country	Germany
Document type	Review ; Journal Article
ZDB-ID	801512-0
ISSN	2567-5761 ; 0720-9355
ISSN (online)	2567-5761
ISSN	0720-9355
DOI	10.1055/a-2178-6491
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Article: The Concept of Thromboinflammation

Schrottmaier, Waltraud C. / Assinger, Alice

Hämostaseologie

2024 Volume 44, Issue 01, Page(s) 21–30

Abstract	Inflammation and thrombosis are intricate and closely interconnected biological processes that are not yet fully understood and lack effective targeted therapeutic approaches. Thrombosis initiated by inflammatory responses, known as immunothrombosis, can confer advantages to the host by constraining the spread of pathogens within the bloodstream. Conversely, platelets and the coagulation cascade can influence inflammatory responses through interactions with immune cells, endothelium, or complement system. These interactions can lead to a state of heightened inflammation resulting from thrombotic processes, termed as thromboinflammation. This review aims to comprehensively summarize the existing knowledge of thromboinflammation and addressing its significance as a challenging clinical issue.
Keywords	thromboinflammation ; immunothrombosis ; platelets ; coagulation ; leukocytes ; complement ; Thromboinflammation ; Immunthrombose ; Blutplättchen ; Gerinnung ; Leukozyten ; Komplement
Language	English
Publishing date	2024-02-01
Publisher	Georg Thieme Verlag KG
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	801512-0
ISSN	2567-5761 ; 0720-9355
ISSN (online)	2567-5761
ISSN	0720-9355
DOI	10.1055/a-2178-6491
Database	Thieme publisher's database

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Article ; Online: Platelet count, temperature and pH value differentially affect hemostatic and immunomodulatory functions of platelets.

Schmuckenschlager, Anna / Pirabe, Anita / Assinger, Alice / Schrottmaier, Waltraud C

Thrombosis research

2023 Volume 223, Page(s) 111–122

Abstract: ... temperature than at 37 °C, incubation temperature did not affect platelet-leukocyte aggregate formation ...

Abstract	Platelets are primarily recognized for their role in hemostasis, but also regulate immune responses by interacting with leukocytes. Their highly sensitive nature enables platelets to rapidly respond to micro-environmental changes, which is crucial under physiological condition but can jeopardize in vitro analyses. Thus, we tested how platelet count and changes in pH and temperatures, which are commonly experienced during inflammation and infection but also affected by ex vivo analyses, influence platelet-leukocyte interaction and immunomodulation. Reducing platelet count by up to 90 % slightly decreased platelet activation and platelet-leukocyte aggregate formation, but did not affect CD11b activation nor CD62L shedding of monocytes or neutrophils. Acidosis (pH 6.9) slightly elevated platelet degranulation and binding to innate leukocytes, though pH changes did not modulate leukocyte activation. While platelet responsiveness was higher at room temperature than at 37 °C, incubation temperature did not affect platelet-leukocyte aggregate formation. In contrast, platelet-mediated CD11b activation and CD62L expression increased with temperature. Our data thus demonstrate the importance of standardized protocols for sample preparation and assay procedure to obtain comparable data. Further, unspecific physiologic responses such as thrombocytopenia, acidosis or temperature changes may contribute to platelet dysfunction and altered platelet-mediated immunomodulation in inflammatory and infectious disease.
MeSH term(s)	Humans ; Temperature ; Platelet Count ; Hemostatics/metabolism ; Blood Platelets/metabolism ; Platelet Activation ; Hemostasis ; Leukocytes/metabolism ; Immunity ; Acidosis/metabolism ; Hydrogen-Ion Concentration
Chemical Substances	Hemostatics
Language	English
Publishing date	2023-01-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	121852-9
ISSN	1879-2472 ; 0049-3848
ISSN (online)	1879-2472
ISSN	0049-3848
DOI	10.1016/j.thromres.2023.01.026
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Article ; Online: Platelets in Viral Infections - Brave Soldiers or Trojan Horses.

Schrottmaier, Waltraud C / Schmuckenschlager, Anna / Pirabe, Anita / Assinger, Alice

Frontiers in immunology

2022 Volume 13, Page(s) 856713

Abstract: Viral infections are often associated with platelet activation and haemostatic complications. In line, low platelet counts represent a hallmark for poor prognosis in many infectious diseases. The underlying cause of platelet dysfunction in viral ... ...

Abstract	Viral infections are often associated with platelet activation and haemostatic complications. In line, low platelet counts represent a hallmark for poor prognosis in many infectious diseases. The underlying cause of platelet dysfunction in viral infections is multifaceted and complex. While some viruses directly interact with platelets and/or megakaryocytes to modulate their function, also immune and inflammatory responses directly and indirectly favour platelet activation. Platelet activation results in increased platelet consumption and degradation, which contributes to thrombocytopenia in these patients. The role of platelets is often bi-phasic. Initial platelet hyper-activation is followed by a state of platelet exhaustion and/or hypo-responsiveness, which together with low platelet counts promotes bleeding events. Thereby infectious diseases not only increase the thrombotic but also the bleeding risk or both, which represents a most dreaded clinical complication. Treatment options in these patients are limited and new therapeutic strategies are urgently needed to prevent adverse outcome. This review summarizes the current literature on platelet-virus interactions and their impact on viral pathologies and discusses potential intervention strategies. As pandemics and concomitant haemostatic dysregulations will remain a recurrent threat, understanding the role of platelets in viral infections represents a timely and pivotal challenge.
MeSH term(s)	Blood Platelets ; Hemostatics ; Humans ; Thrombocytopenia ; Virus Diseases ; Viruses
Chemical Substances	Hemostatics
Language	English
Publishing date	2022-03-28
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.856713
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Article ; Online: Direct and indirect effects of Puumala hantavirus on platelet function.

Schrottmaier, Waltraud C / Schmuckenschlager, Anna / Thunberg, Therese / Wigren-Byström, Julia / Fors-Connolly, Anne-Marie / Assinger, Alice / Ahlm, Clas / Forsell, Mattias N E

Thrombosis research

2023 Volume 233, Page(s) 41–54

Abstract: Thrombocytopenia is a cardinal symptom of hantavirus-induced diseases including Puumala virus (PUUV)-induced hemorrhagic fever with renal syndrome (HFRS), which is associated with impaired platelet function, bleeding manifestations and augmented ... ...

Abstract	Thrombocytopenia is a cardinal symptom of hantavirus-induced diseases including Puumala virus (PUUV)-induced hemorrhagic fever with renal syndrome (HFRS), which is associated with impaired platelet function, bleeding manifestations and augmented thrombotic risk. However, the underlying mechanisms causing thrombocytopenia and platelet hypo-responsiveness are unknown. Thus, we investigated the direct and indirect impact of PUUV on platelet production, function and degradation. Analysis of PUUV-HFRS patient blood revealed that platelet hypo-responsiveness in PUUV infection was cell-intrinsic and accompanied by reduced platelet-leukocyte aggregates (PLAs) and upregulation of monocyte tissue factor (TF), whereas platelet vasodilator-stimulated phosphoprotein (VASP) phosphorylation was comparable to healthy controls. Plasma CXCL4 levels followed platelet count dynamics throughout disease course. PUUV activated both neutrophils and monocytes in vitro, but platelet desialylation, degranulation and GPIIb/IIIa activation as well as PLA formation and endothelial adhesion under flow remained unaltered in the presence of PUUV. Further, MEG-01 megakaryocytes infected with PUUV displayed unaltered polyploidization, expression of surface receptors and platelet production. However, infection of endothelial cells with PUUV significantly increased platelet sequestration. Our data thus demonstrate that although platelet production, activation or degradation are not directly modulated, PUUV indirectly fosters thrombocytopenia by sequestration of platelets to infected endothelium. Upregulation of immunothrombotic processes in PUUV-HFRS may further contribute to platelet dysfunction and consumption. Given the pathophysiologic similarities of hantavirus infections, our findings thus provide important insights into the mechanisms underlying thrombocytopenia and highlight immune-mediated coagulopathy as potential therapeutic target.
MeSH term(s)	Humans ; Puumala virus ; Hemorrhagic Fever with Renal Syndrome/diagnosis ; Hemorrhagic Fever with Renal Syndrome/therapy ; Endothelial Cells ; Orthohantavirus ; Thrombocytopenia
Language	English
Publishing date	2023-11-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	121852-9
ISSN	1879-2472 ; 0049-3848
ISSN (online)	1879-2472
ISSN	0049-3848
DOI	10.1016/j.thromres.2023.11.017
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Article: PI3K Isoform Signalling in Platelets.

Schrottmaier, Waltraud C / Mussbacher, Marion / Salzmann, Manuel / Kral-Pointner, Julia B / Assinger, Alice

Current topics in microbiology and immunology

2022 Volume 436, Page(s) 255–285

Abstract: Platelets are unique anucleated blood cells that constantly patrol the vasculature to seal and prevent injuries in a process termed haemostasis. Thereby they rapidly adhere to the subendothelial matrix and recruit further platelets, resulting in platelet ...

Abstract	Platelets are unique anucleated blood cells that constantly patrol the vasculature to seal and prevent injuries in a process termed haemostasis. Thereby they rapidly adhere to the subendothelial matrix and recruit further platelets, resulting in platelet aggregates. Apart from their central role in haemostasis, they also kept some of their features inherited by their evolutionary ancestor-the haemocyte, which was also involved in immune defences. Together with leukocytes, platelets fight pathogenic invaders and guide many immune processes. In addition, they rely on several signalling pathways which are also relevant to immune cells. Among these, one of the central signalling hubs is the PI3K pathway. Signalling processes in platelets are unique as they lack a nucleus and therefore transcriptional regulation is absent. As a result, PI3K subclasses fulfil distinct roles in platelets compared to other cells. In contrast to leukocytes, the central PI3K subclass in platelet signalling is PI3K class Iβ, which underlines the uniqueness of this cell type and opens new ways for potential platelet-specific pharmacologic inhibition. An overview of platelet function and signalling with emphasis on PI3K subclasses and their respective inhibitors is given in this chapter.
MeSH term(s)	Blood Platelets/metabolism ; Blood Platelets/pathology ; Hemostasis/physiology ; Humans ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Isoforms/metabolism ; Thrombosis/metabolism ; Thrombosis/pathology
Chemical Substances	Protein Isoforms
Language	English
Publishing date	2022-10-15
Publishing country	Germany
Document type	Journal Article
ISSN	0070-217X
ISSN	0070-217X
DOI	10.1007/978-3-031-06566-8_11
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Article ; Online: Age-Dependent Surface Receptor Expression Patterns in Immature Versus Mature Platelets in Mouse Models of Regenerative Thrombocytopenia.

Pirabe, Anita / Frühwirth, Sabine / Brunnthaler, Laura / Hackl, Hubert / Schmuckenschlager, Anna / Schrottmaier, Waltraud C / Assinger, Alice

Cells

2023 Volume 12, Issue 19

Abstract: Aging is a multifaceted process that unfolds at both the individual and cellular levels, resulting in changes in platelet count and platelet reactivity. These alterations are influenced by shifts in platelet production, as well as by various ... ...

Abstract	Aging is a multifaceted process that unfolds at both the individual and cellular levels, resulting in changes in platelet count and platelet reactivity. These alterations are influenced by shifts in platelet production, as well as by various environmental factors that affect circulating platelets. Aging also triggers functional changes in platelets, including a reduction in RNA content and protein production capacity. Older individuals and RNA-rich immature platelets often exhibit hyperactivity, contributing significantly to pathologic conditions such as cardiovascular diseases, sepsis, and thrombosis. However, the impact of aging on surface receptor expression of circulating platelets, particularly whether these effects vary between immature and mature platelets, remains largely unexplored. Thus, we investigated the expression of certain surface and activation receptors on platelets from young and old mice as well as on immature and mature platelets from mouse models of regenerative thrombocytopenia by flow cytometry. Our findings indicate that aged mice show an upregulated expression of the platelet endothelial cell adhesion molecule-1 (CD31), tetraspanin-29 (CD9), and Toll-like receptor 2 (TLR2) compared to their younger counterparts. Interestingly, when comparing immature and mature platelets in both young and old mice, no differences were observed in mature platelets. However, immature platelets from young mice displayed higher surface expression compared to immature platelets from old mice. Additionally, in mouse models of regenerative thrombocytopenia, the majority of receptors were upregulated in immature platelets. These results suggest that distinct surface receptor expressions are increased on platelets from old mice and immature platelets, which may partially explain their heightened activity and contribute to an increased thrombotic risk.
MeSH term(s)	Mice ; Animals ; Receptor for Advanced Glycation End Products/metabolism ; Blood Platelets/metabolism ; Thrombocytopenia/metabolism ; Platelet Count ; RNA/metabolism
Chemical Substances	Receptor for Advanced Glycation End Products ; RNA (63231-63-0)
Language	English
Publishing date	2023-10-08
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12192419
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Article ; Online: Reduced Monocyte and Neutrophil Infiltration and Activation by P-Selectin/CD62P Inhibition Enhances Thrombus Resolution in Mice.

Kral-Pointner, Julia B / Haider, Patrick / Szabo, Petra L / Salzmann, Manuel / Brekalo, Mira / Schneider, Karl H / Schrottmaier, Waltraud C / Kaun, Christoph / Bleichert, Sonja / Kiss, Attila / Sickha, Romana / Hengstenberg, Christian / Huber, Kurt / Brostjan, Christine / Bergmeister, Helga / Assinger, Alice / Podesser, Bruno K / Wojta, Johann / Hohensinner, Philipp

Arteriosclerosis, thrombosis, and vascular biology

2024 Volume 44, Issue 4, Page(s) 954–968

Abstract: Background: Venous thromboembolism is a major health problem. After thrombus formation, its resolution is essential to re-establish blood flow, which is crucially mediated by infiltrating neutrophils and monocytes in concert with activated platelets and ...

Abstract	Background: Venous thromboembolism is a major health problem. After thrombus formation, its resolution is essential to re-establish blood flow, which is crucially mediated by infiltrating neutrophils and monocytes in concert with activated platelets and endothelial cells. Thus, we aimed to modulate leukocyte function during thrombus resolution post-thrombus formation by blocking P-selectin/CD62P-mediated cell interactions. Methods: Thrombosis was induced by inferior vena cava stenosis through ligation in mice. After 1 day, a P-selectin-blocking antibody or isotype control was administered and thrombus composition and resolution were analyzed. Results: Localizing neutrophils and macrophages in thrombotic lesions of wild-type mice revealed that these cells enter the thrombus and vessel wall from the caudal end. Neutrophils were predominantly present 1 day and monocytes/macrophages 3 days after vessel ligation. Blocking P-selectin reduced circulating platelet-neutrophil and platelet-Ly6C Conclusions: Inhibition of P-selectin-dependent activation of monocytes and neutrophils accelerates venous thrombosis resolution due to reduced infiltration and activation of innate immune cells at the site of thrombus formation, which prevents early thrombus stabilization and facilitates fibrinolysis.
MeSH term(s)	Mice ; Humans ; Animals ; Monocytes/pathology ; P-Selectin ; Endothelial Cells ; Thromboplastin ; Neutrophil Infiltration ; Thrombosis ; Neutrophils
Chemical Substances	P-Selectin ; Thromboplastin (9035-58-9)
Language	English
Publishing date	2024-02-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.123.320016
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Article ; Online: Platelet-leukocyte interplay during vascular disease.

Schrottmaier, Waltraud C / Mussbacher, Marion / Salzmann, Manuel / Assinger, Alice

Atherosclerosis

2020 Volume 307, Page(s) 109–120

Abstract: Vascular disease is a progressive inflammatory condition fuelled by an unhealthy lifestyle of physical inactivity, cholesterol-rich diet, and smoking. Together with endogenous factors such as age, gender, and autoimmune status, an unhealthy lifestyle ... ...

Abstract	Vascular disease is a progressive inflammatory condition fuelled by an unhealthy lifestyle of physical inactivity, cholesterol-rich diet, and smoking. Together with endogenous factors such as age, gender, and autoimmune status, an unhealthy lifestyle fosters a pro-inflammatory and pro-thrombotic milieu, which can lead to endothelial dysfunction, atherosclerotic plaque formation and vascular obstruction or degradation of the subendothelial matrix. Platelet-leukocyte interplay represents an important feature in this context. Platelets get activated in a pro-inflammatory and pro-thrombotic microenvironment and readily interact with innate and adaptive immune cells alike. Even though platelet affinity for physical cell-cell contact is highest with monocytes/macrophages and neutrophils, platelets also avidly interact with lymphocytes by soluble mediators. Platelet-leukocyte crosstalk regulates essential immune responses, supporting leukocyte recruitment at sites of vascular insult, promoting proliferation and differentiation of leukocytes and enhancing pro-inflammatory effector functions such as cytokine and reactive oxygen production. However, under certain conditions platelet-leukocyte interplay also dampens the inflammatory process. Crosstalk of platelet and leukocytes thus represents a driving force in vascular disease. In this review, we highlight the impact of various risk factors for vascular disease on platelet-leukocyte interactions and discuss the underlying mechanisms of platelet-mediated changes in immune responses and the effect of immune cells on the haemostatic system. As the underlying pathologies differ between vascular diseases, we summarize our current knowledge on platelet-leukocyte interplay in chronic vascular diseases such as abdominal aortic aneurysm, peripheral and coronary artery disease as well as acute vascular diseases such as ischaemic stroke and venous thromboembolism.
MeSH term(s)	Blood Platelets ; Brain Ischemia ; Humans ; Inflammation ; Leukocytes ; Neutrophils ; Stroke
Language	English
Publishing date	2020-05-11
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2020.04.018
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Article: Horizontal MicroRNA Transfer by Platelets - Evidence and Implications.

Mussbacher, Marion / Pirabe, Anita / Brunnthaler, Laura / Schrottmaier, Waltraud C / Assinger, Alice

Frontiers in physiology

2021 Volume 12, Page(s) 678362

Abstract: For decades, platelets have been known for their central role in hemostasis and their ability to release bioactive molecules, allowing inter-platelet communication and crosstalk with the immune system and vascular cells. However, with the detection of ... ...

Abstract	For decades, platelets have been known for their central role in hemostasis and their ability to release bioactive molecules, allowing inter-platelet communication and crosstalk with the immune system and vascular cells. However, with the detection of microRNAs in platelets and platelet-derived microvesicles (MVs), a new level of inter-cellular regulation was revealed. By shedding MVs from their plasma membrane, platelets are able to release functional microRNA complexes that are protected from plasma RNases. Upon contact with macrophages, endothelial cells and smooth muscle cells platelet microRNAs are rapidly internalized and fine-tune the functionality of the recipient cell by post-transcriptional reprogramming. Moreover, microRNA transfer by platelet MVs allows infiltration into tissues with limited cellular access such as solid tumors, thereby they not only modulate tumor progression but also provide a potential route for drug delivery. Understanding the precise mechanisms of horizontal transfer of platelet microRNAs under physiological and pathological conditions allows to design side-specific therapeutic (micro)RNA delivery systems. This review summarizes the current knowledge and the scientific evidence of horizontal microRNA transfer by platelets and platelet-derived MVs into vascular and non-vascular cells and its physiological consequences.
Language	English
Publishing date	2021-06-03
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2021.678362
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