The Complement C5a-C5aR1 GPCR Axis in COVID-19 Therapeutics [PDF]
The current pandemic of coronavirus disease (COVID-19) caused by SARS-CoV-2 is a significant global health challenge. A recent study by Carvelli and colleagues now demonstrates the involvement of complement C5a and its receptor C5aR1 in disease progression and suggests that blockade of the C5a-C5aR1 axis may represent a potential therapeutic strategy ...
Woodruff, Trent M., Shukla, Arun K.
core +8 more sources
Therapeutic Potential of Targeting Complement C5a Receptors in Diabetic Kidney Disease [PDF]
Diabetic kidney disease (DKD) affects 30–40% of patients with diabetes and is currently the leading cause of end-stage renal disease (ESRD). The activation of the complement cascade, a highly conserved element of the innate immune system, has been ...
Sih Min Tan +2 more
core +2 more sources
New insights for C5a and C5a receptors in sepsis [PDF]
The complement system plays a central role in inflammation and immunity. Among the complement activation products, C5a is one of the most potent inflammatory peptides with a broad spectrum of functions.
Hongwei eGao, Chunguang eYan
doaj +2 more sources
Functional Analysis of a Novel Complement C5a Receptor 1-Blocking Monoclonal Antibody [PDF]
Introduction: The complement system anaphylatoxin C5a is a critical player in inflammation. By binding to complement C5a receptor 1 (C5aR1/CD88), C5a regulates many cellular functions, mainly as a potent pro-inflammatory inducer.
Leon Cyranka +6 more
doaj +2 more sources
Complement C5a receptors in the pituitary gland: expression and function [PDF]
Communication between the immune and endocrine system is important for the control of inflammation that is primarily mediated through the hypothalamic–pituitary–adrenal axis. The innate immune system rapidly responds to pathogens by releasing complement proteins that include the anaphylatoxins C3a and C5a.
Karen, Francis +3 more
openaire +3 more sources
Complement Anaphylatoxin C5a, Endothelial Dysfunction and Low-Grade Inflammation in Atherosclerotic Vascular Diseases [PDF]
Objectives: The objective of the paper is to summarize the evidence in atherosclerosis research regarding the relationship of complement C5a with low-grade inflammation, endothelial dysfunction, and atherosclerosis.
Gansuvd Shagdarsuren +4 more
doaj +2 more sources
Complement Factor C5a Inhibits Apoptosis of Neutrophils—A Mechanism in Polytrauma? [PDF]
Life-threatening polytrauma results in early activation of the complement and apoptotic system, as well as leukocytes, ultimately leading to the clearance of damaged cells. However, little is known about interactions between the complement and apoptotic systems in PMN (polymorphonuclear neutrophils) after multiple injuries. PMN from polytrauma patients
Christian Ehrnthaller +5 more
openaire +4 more sources
Complement C5a Receptor Signaling Alters Stress Responsiveness and Modulates Microglia Following Chronic Stress Exposure [PDF]
Background: Accumulating evidence underscores the pivotal role of heightened inflammation in the pathophysiology of stress-related diseases, but the underlying mechanisms remain elusive.
Hsiao-Jou Cortina Chen +7 more
doaj +2 more sources
Role of complement C5a and histones in septic cardiomyopathy [PDF]
Polymicrobial sepsis (after cecal ligation and puncture, CLP) causes robust complement activation with release of C5a. Many adverse events develop thereafter and will be discussed in this review article. Activation of complement system results in generation of C5a which interacts with its receptors (C5aR1, C5aR2).
Fatemeh Fattahi +7 more
openaire +4 more sources
Complement C5a‐Induced Changes in Neutrophil Morphology During Inflammation [PDF]
AbstractThe complement and neutrophil defence systems, as major components of innate immunity, are activated during inflammation and infection. For neutrophil migration to the inflamed region, we hypothesized that the complement activation product C5a induces significant changes in cellular morphology before chemotaxis. Exposure of human neutrophils to
S. Denk +16 more
openaire +3 more sources

