ReviewClinical and experimental medicine2018
The role of the alternative pathway of complement activation in glomerular diseases.
Review in Clinical and experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 75 citations in OpenAlex.
- The Alternative Complement Pathway in IgA Nephropathy: A Podcast for Advanced Practice Providers.Advances in therapy · 2026Article
- Atypical Hemolytic Uremic Syndrome With Hypocellular Bone Marrow: A Report of a Rare Case.Cureus · 2026Article
- CFD protein deficiency induce slow transit constipation is correlated with gut microbial dysbiosis.Scientific reports · 2026Article
- Article
- Research progress on the lectin pathway of complement in IgA nephropathy.Frontiers in immunology · 2026Review
- Perfluorooctanoic acid-associated complement factor B upregulation and atrial fibrillation-related molecular alterations: integrated network toxicology, Mendelian randomization, molecular dynamics, and HL-1 cell analyses.Frontiers in cardiovascular medicine · 2026Article
- Myocardial phosphoproteomics unveils a key role of DYRK1A in aortic valve replacement-induced reverse remodelling.Basic research in cardiology · 2025Article
- Emerging role of complement system in the induction of neuroinflammation in adenylosuccinate lyase deficiency disorder.Brain, behavior, & immunity - health · 2025Review
- Spatially resolved transcriptomic profiling for glomerular and tubulointerstitial gene expression in C3 glomerulopathy.Clinical kidney journal · 2025Article
- Factor B as a therapeutic target for the treatment of complement-mediated diseases.Frontiers in immunology · 2025Review
- Complement System and Adhesion Molecule Skirmishes in Fabry Disease: Insights into Pathogenesis and Disease Mechanisms.International journal of molecular sciences · 2024Review
- SARS-CoV-2 Protein Deposition Enhances Renal Complement Activation and Aggravates Kidney Injury in Membranous Nephropathy After COVID-19.Kidney international reports · 2024Article
- The prognostic role of activation of the complement pathways in the progression of advanced IgA nephropathy to end-stage renal disease.BMC nephrology · 2024Article
- Complement C3a/C3aR and C5a/C5aR deposits accelerate the progression of advanced IgA nephropathy to end-stage renal disease.Clinical and experimental medicine · 2024Article
- C3d-Targeted factor H inhibits tissue complement in disease models and reduces glomerular injury without affecting circulating complement.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Adipsin in the pathogenesis of cardiovascular diseases.Vascular pharmacology · 2024Review
- Gliosis-dependent expression of complement factor H truncated variants attenuates retinal neurodegeneration following ischemic injury.Journal of neuroinflammation · 2024Article
- The Relationship between Complements and Age-Related Macular Degeneration and Its Pathogenesis.Journal of ophthalmology · 2024Review
- Functional evaluation of rare variants in complement factor I using a minigene assay.Frontiers in immunology · 2024Article
- Diagnostic Problems in C3 Glomerulopathy.Biomedicines · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement system (CS) has recently been recognized as a bridge between innate and adaptive immunity that constitutes a very complex mechanism controlling the clearance of pathogens, cellular debris, and immune complexes. Out of three known pathways of complement activation, the alternative pathway (AP) plays a critical role in host defense by amplifying the complement response, independently of initiation pathway and continuously maintaining low-level activity in a process called 'thick-over.' A key molecule of the CS is C3, in which the AP is constantly activated. To prevent host cell destruction, a group of the AP regulators tightly controls this pathway of the CS activation. Acquired and genetic abnormalities of the CS may alter the delicate balance between enhancing and inhibiting the AP cascade. These can lead to the uncontrolled CS activation, inflammatory response, and subsequent tissue damage. Since complement components are locally produced and activated in the kidney, the abnormalities targeting the AP may cause glomerular injury. C3 glomerulopathy is a new entity, in which the AP dysregulation has been well established. However, recent studies indicate that the AP may also contribute to a wide range of kidney pathologies, including immune-complex-mediated glomerulonephritis (GN), pauci-immune GN, and primary membranous nephropathy (PMN). This article provides insight into current knowledge on the role of the AP in the pathogenesis of glomerular diseases, focusing mainly on various types of primary and secondary GN and PMN.
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