Liver Cirrhosis, Experimental
|
0.300 |
Biomarker
|
disease |
CTD_human |
Systems level analysis and identification of pathways and networks associated with liver fibrosis.
|
25380136 |
2014 |
Endotoxic shock
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Disruption of the C5a receptor gene increases resistance to acute Gram-negative bacteremia and endotoxic shock: opposing roles of C3a and C5a.
|
18063050 |
2008 |
Septic Shock
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
Disruption of the C5a receptor gene increases resistance to acute Gram-negative bacteremia and endotoxic shock: opposing roles of C3a and C5a.
|
18063050 |
2008 |
Toxic Shock Syndrome
|
0.300 |
Biomarker
|
disease |
CTD_human |
Disruption of the C5a receptor gene increases resistance to acute Gram-negative bacteremia and endotoxic shock: opposing roles of C3a and C5a.
|
18063050 |
2008 |
Sepsis
|
0.290 |
Biomarker
|
disease |
BEFREE |
We recently discovered that C5aR1 exacerbates the course of the disease, revealing a downside of complement in <i>Nme</i> sepsis.
|
31274379 |
2019 |
Sepsis
|
0.290 |
Biomarker
|
disease |
BEFREE |
MEDI7814 has therapeutic potential for the treatment of acute inflammatory conditions in which both C5a receptors may mediate inflammation, such as sepsis or renal ischemia-reperfusion injury.
|
28952876 |
2018 |
Sepsis
|
0.290 |
Biomarker
|
disease |
BEFREE |
Together, these data emphasize the role of complement (C5a) and C5a receptors (C5aR1, C5aR2), as well as extracellular histones in events that lead to cardiac dysfunction of sepsis (septic cardiomyopathy).
|
29914696 |
2018 |
Sepsis
|
0.290 |
Biomarker
|
disease |
BEFREE |
C5a, C5aR, and NF-κB, which were shown to be the key molecules in brain injury pathogenesis in sepsis, might also be utilized as potential targets for future treatment trials of septic encephalopathy.
|
29232196 |
2018 |
Sepsis
|
0.290 |
Biomarker
|
disease |
BEFREE |
Together, our findings demonstrate that C5aR1 drives the pathophysiology associated with meningococcal sepsis and provides a promising target for adjunctive therapy.<b>IMPORTANCE</b> The devastating consequences of <i>N. meningitidis</i> sepsis arise due to the rapidly arising and self-propagating inflammatory response that mobilizes antibacterial defenses but also drives the immunopathology associated with meningococcemia.
|
29362231 |
2018 |
Sepsis
|
0.290 |
Biomarker
|
disease |
BEFREE |
Our studies, using in vivo and in vitro models, have demonstrated that C5a and its receptors (C5aR1 and C5aR2) play key roles in cardiac dysfunction developing during sepsis.
|
27931779 |
2017 |
Sepsis
|
0.290 |
Biomarker
|
disease |
BEFREE |
Complement 5a (C5a) has been implicated in the pathogenesis of sepsis by inducing the functional impairment of neutrophils; however, the utility of C5a receptors (C5aRs; C5aR and C5L2) as biomarkers for the management of sepsis is uncertain.
|
25726869 |
2016 |
Sepsis
|
0.290 |
Biomarker
|
disease |
RGD |
The complement anaphylatoxin C5a induces apoptosis in adrenomedullary cells during experimental sepsis.
|
18648551 |
2008 |
Sepsis
|
0.290 |
GeneticVariation
|
disease |
BEFREE |
During experimental sepsis in rodents after cecal ligation and puncture (CLP), excessive C5a is generated, leading to interactions with C5aR, loss of innate immune functions of neutrophils, and lethality.
|
15784721 |
2005 |
Sepsis
|
0.290 |
ModifyingMutation
|
disease |
RGD |
Neutrophil C5a receptor and the outcome in a rat model of sepsis.
|
12897064 |
2003 |
Sepsis
|
0.290 |
AlteredExpression
|
disease |
BEFREE |
These results demonstrate the expression of C3aR and C5aR by cells endogenous to the lung, and, given the participation of bronchial epithelial and smooth muscle cells in the pathology of diseases such as sepsis and asthma, the data suggest a role for these receptors during lung inflammation.
|
11160252 |
2001 |
Asthma
|
0.270 |
AlteredExpression
|
disease |
BEFREE |
RSV enhanced lung damage, airway hyperresponsiveness, and C5aR expressions in asthma mice, while C5aRA alleviated these pathologic changes.
|
29123203 |
2017 |
Asthma
|
0.270 |
Biomarker
|
disease |
RGD |
Use of monoclonal antibodies to assess expression of anaphylatoxin receptors in rat and murine models of lung inflammation.
|
17544263 |
2007 |
Asthma
|
0.270 |
Biomarker
|
disease |
LHGDN |
Contribution of anaphylatoxins to allergic inflammation in human lungs.
|
16301808 |
2005 |
Asthma
|
0.270 |
GeneticVariation
|
disease |
BEFREE |
To determine whether genetic variations in the genes of the complement system affect susceptibility to BA, we screened single nucleotide polymorphisms (SNPs) in C3, C5, the C3a receptor gene (C3AR1), and the C5a receptor gene (C5R1) and performed association studies in the Japanese population.
|
15278436 |
2004 |
Asthma
|
0.270 |
GeneticVariation
|
disease |
BEFREE |
The aim of this study was to screen for novel polymorphisms in the C5R1 gene and to determine whether any identified polymorphisms are associated with asthma and/or atopy and whether they are functional.
|
15144465 |
2004 |
Asthma
|
0.270 |
AlteredExpression
|
disease |
LHGDN |
Complement factors c3a, c4a, and c5a in chronic obstructive pulmonary disease and asthma.
|
15039137 |
2004 |
Asthma
|
0.270 |
AlteredExpression
|
disease |
BEFREE |
These results demonstrate the expression of C3aR and C5aR by cells endogenous to the lung, and, given the participation of bronchial epithelial and smooth muscle cells in the pathology of diseases such as sepsis and asthma, the data suggest a role for these receptors during lung inflammation.
|
11160252 |
2001 |
Asthma
|
0.270 |
Biomarker
|
disease |
BEFREE |
Blockade of the C5a receptor rendered human monocytes unable to produce IL-12, mimicking blunted IL-12 production by macrophages from C5-deficient mice and providing a mechanism for the regulation of susceptibility to asthma by C5.
|
10973279 |
2000 |
Amyotrophic Lateral Sclerosis
|
0.240 |
AlteredExpression
|
disease |
BEFREE |
These results indicate that similar to SOD1 transgenic animals, local complement activation and increased expression of C5aR1 may contribute to motor neuron death and neuromuscular junction denervation in the TDP-43<sup>Q331K</sup> mouse ALS model.
|
29859100 |
2018 |
Amyotrophic Lateral Sclerosis
|
0.240 |
Biomarker
|
disease |
BEFREE |
Importantly, genetic or pharmacological blockage of C5aR1 improves motor performance and reduces disease pathology in hSOD1<sup>G93A</sup> rodent models of ALS.
|
28571586 |
2017 |