2021
DOI: 10.1016/bs.ai.2021.09.001
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Renal diseases and the role of complement: Linking complement to immune effector pathways and therapeutics

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Cited by 11 publications
(14 citation statements)
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“…Scholars have made considerable progress in understanding the interactions between autophagy and the immune response. Complement is an important part of the innate immune system, and their defects, dysfunction, and abnormal activation are involved in the occurrence and development of a variety of diseases ( Freiwald and Afzali, 2021 ). The complement system is a highly complex biological reaction system that is activated by the classical pathway, alternative pathway, or lectin pathway ( Skinner et al, 2021 ).…”
Section: Discussionmentioning
confidence: 99%
“…Scholars have made considerable progress in understanding the interactions between autophagy and the immune response. Complement is an important part of the innate immune system, and their defects, dysfunction, and abnormal activation are involved in the occurrence and development of a variety of diseases ( Freiwald and Afzali, 2021 ). The complement system is a highly complex biological reaction system that is activated by the classical pathway, alternative pathway, or lectin pathway ( Skinner et al, 2021 ).…”
Section: Discussionmentioning
confidence: 99%
“…Some of the main classes of such complement‐driven diseases are nephropathies, where complement is directly deposited on kidney surfaces, and thrombotic microangiopathies (TMAs), characterized by intravascular hemolysis, clotting, and kidney damage via immune‐complex accumulation (See Table 3 below and refs 110–112). Kidney diseases are highly prevalent and can be classified as chronic kidney disease (decreased renal function for over 3 months) and acute kidney injury (reduced kidney function occurs over a shorter period, up to few weeks) 110 . One example of the latter is acute postinfectious glomerulonephritis (APIGN), a disease that typically follows streptococcal infection and is characterized by low C3 and normal C4 levels in blood, suggesting AP involvement.…”
Section: Disease Amenable To C3 Inhibitionmentioning
confidence: 99%
“…aHUS is a term used to describe all TMAs, which are not caused by Shiga‐toxin or ADAMTS13 deficiency, and are instead caused by loss of regulation of the complement cascade (See Table 3 and ref. 110). These disorders are generally characterized by thrombocytopenia, hemolytic anemia, and thrombosis in the microvasculature 118 …”
Section: Disease Amenable To C3 Inhibitionmentioning
confidence: 99%
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