Update on the role of endothelial cells in trauma

Greven, Johannes; Pfeifer, Rolf; Zhi, Qi; Pape, Hans-Christian

doi:10.1007/s00068-017-0812-8

Cited by 20 publications

(18 citation statements)

References 134 publications

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“…, Greven et al . ). APC was initially thought to be the primary driver of hyperfibrinolysis in ATC through inhibition of PAI‐1, but this has recently been called into question.…”

Section: Acquired Hyperfibrinolysismentioning

confidence: 97%

“…Three distinct fibrinolytic phenotypes are reported in people with acute traumatic coagulopathy: hyperfibrinolysis, physiological fibrinolysis and shutdown of fibrinolysis (Moore et al 2014). Hyperfibrinolysis, as seen in ATC, occurs when trauma and hypoperfusion (shock) result in endothelial cell activation and glycocalyx dysfunction, platelet dysfunction, increased systemic tPA and activation of protein C , Johansson et al 2012, Wohlauer et al 2012, Chapman et al 2016, Greven et al 2018. APC was initially thought to be the primary driver of hyperfibrinolysis in ATC through inhibition of PAI-1, but this has recently been called into question.…”

Section: Acute Traumatic Coagulopathymentioning

confidence: 99%

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A review of hyperfibrinolysis in cats and dogs

Birkbeck

Humm

Cortellini

2019

J of Small Animal Practice

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The fibrinolytic system is activated concurrently with coagulation; it regulates haemostasis and prevents thrombosis by restricting clot formation to the area of vascular injury and dismantling the clot as healing occurs. Dysregulation of the fibrinolytic system, which results in hyperfibrinolysis, may manifest as clinically important haemorrhage. Hyperfibrinolysis occurs in cats and dogs secondary to a variety of congenital and acquired disorders. Acquired disorders associated with hyperfibrinolysis, such as trauma, cavitary effusions, liver disease and Angiostrongylus vasorum infection, are commonly encountered in primary care practice. In addition, delayed haemorrhage reported in greyhounds following trauma and routine surgical procedures has been attributed to a hyperfibrinolytic disorder, although this has yet to be characterised. The diagnosis of hyperfibrinolysis is challenging and, until recently, has relied on techniques that are not readily available outside referral hospitals. With the recent development of point‐of‐care viscoelastic techniques, assessment of fibrinolysis is now possible in referral practice. This will provide the opportunity to target haemorrhage due to hyperfibrinolysis with antifibrinolytic drugs and thereby reduce associated morbidity and mortality. The fibrinolytic system and the conditions associated with increased fibrinolytic activity in cats and dogs are the focus of this review article. In addition, laboratory and point‐of‐care techniques for assessing hyperfibrinolysis and antifibrinolytic treatment for patients with haemorrhage are reviewed.

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“…, Greven et al . ). APC was initially thought to be the primary driver of hyperfibrinolysis in ATC through inhibition of PAI‐1, but this has recently been called into question.…”

Section: Acquired Hyperfibrinolysismentioning

confidence: 97%

Section: Acute Traumatic Coagulopathymentioning

confidence: 99%

A review of hyperfibrinolysis in cats and dogs

Birkbeck

Humm

Cortellini

2019

J of Small Animal Practice

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“…In general, circulating levels of S100B in severely injured trauma patients were increased as compared to healthy volunteers [206]. Even more, S100B levels correlated with systemic levels of sE-selectin and von willebrand factor, which are indicating endothelial cell injury [206,209]. Further mechanistical analyses of human endothelial cells transfected with S100B uncovered an increase in apoptosis and levels of proinflammatory cytokines IL-6 and IL-8 [206].…”

Section: S100a Proteinsmentioning

confidence: 99%

Damage-associated molecular patterns in trauma

Relja

Land

2019

Eur J Trauma Emerg Surg

139

131

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In 1994, the "danger model" argued that adaptive immune responses are driven rather by molecules released upon tissue damage than by the recognition of "strange" molecules. Thus, an alternative to the "self versus non-self recognition model" has been provided. The model, which suggests that the immune system discriminates dangerous from safe molecules, has established the basis for the future designation of damage-associated molecular patterns (DAMPs), a term that was coined by Walter G. Land, Seong, and Matzinger. The pathological importance of DAMPs is barely somewhere else evident as in the posttraumatic or post-surgical inflammation and regeneration. Since DAMPs have been identified to trigger specific immune responses and inflammation, which is not necessarily detrimental but also regenerative, it still remains difficult to describe their "friend or foe" role in the posttraumatic immunogenicity and healing process. DAMPs can be used as biomarkers to indicate and/or to monitor a disease or injury severity, but they also may serve as clinically applicable parameters for optimized indication of the timing for, i.e., secondary surgeries. While experimental studies allow the detection of these biomarkers on different levels including cellular, tissue, and circulatory milieu, this is not always easily transferable to the human situation. Thus, in this review, we focus on the recent literature dealing with the pathophysiological importance of DAMPs after traumatic injury. Since dysregulated inflammation in traumatized patients always implies disturbed resolution of inflammation, so-called model of suppressing/inhibiting inducible DAMPs (SAMPs) will be very briefly introduced. Thus, an update on this topic in the field of trauma will be provided.

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“…Additionally, a comparison with mildly injured trauma patients has shown that S100B concentrations were associated with injury severity [172]. S100B levels correlated with systemic levels of sE-selectin, and Von Willebrand factor (vWF), which are indicating endothelial cell injury [172, 175]. Additional mechanistical analyses represented that transfection of human endothelial cells with pcDNA3.1-S100B resulted in increased apoptosis and enhanced levels of proinflammatory IL-6 and IL-8 [172].…”

Section: Danger Signals In Traumamentioning

confidence: 99%

Danger signals in trauma

Relja

Mörs

Marzi

2018

Eur J Trauma Emerg Surg

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This review summarizes a short list of currently discussed trauma-induced danger-associated molecular patterns (DAMP). Due to the bivalent character and often pleiotropic effects of a DAMP, it is difficult to describe its “friend or foe” role in post-traumatic inflammation and regeneration, both systemically as well locally in tissues. DAMP can be used as biomarkers to indicate or monitor disease or injury severity, but also may serve as clinically applicable parameters for better indication and timing of surgery. Due to the inflammatory processes at the local tissue level or the systemic level, the precise role of DAMP is not always clear to define. While in vitro and experimental studies allow for the detection of these biomarkers at the different levels of an organism—cellular, tissue, circulation—this is not always easily transferable to the human setting. Increased knowledge exploring the dual role of DAMP after trauma, and concentrating on their nuclear functions, transcriptional targets, release mechanisms, cellular sources, multiple functions, their interactions and potential therapeutic targeting is warranted.

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Update on the role of endothelial cells in trauma

Abstract: The endothelium is one of the first barriers that comes into contact with exo- and endogenous trauma-related signals and is a pivotal point in activating subsequent pathways and cascades by transfer of information.

Cited by 20 publications

References 134 publications

A review of hyperfibrinolysis in cats and dogs

A review of hyperfibrinolysis in cats and dogs

Damage-associated molecular patterns in trauma

Danger signals in trauma

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