Inflammaging and Complement System: A Link Between Acute Kidney Injury and Chronic Graft Damage
Open accessAbstract
The aberrant activation of complement system in several kidney diseases suggests that this pillar of innate immunity has a critical role in the pathophysiology of renal damage of different etiologies. A growing body of experimental evidence indicates that complement activation contributes to the pathogenesis of acute kidney injury (AKI) such as delayed graft function (DGF) in transplant patients. AKI is characterized by the rapid loss of the kidney’s excretory function and is a complex syndrome currently lacking a specific medical treatment to arrest or attenuate progression in chronic kidney disease (CKD). Recent evidence suggests that independently from the initial trigger (i.e., sepsis or ischemia/reperfusions injury), an episode of AKI is strongly associated with an increased risk of subsequent CKD. The AKI-to-CKD transition may involve a wide range of mechanisms including scar-forming myofibroblasts generated from different sources, microvascular rarefaction, mitochondrial dysfunction, or cell cycle arrest by the involvement of epigenetic, gene, and protein alterations leading to common final signaling pathways [i.e., transforming growth factor beta (TGF-β), p16ink 4 a, Wnt/β-catenin pathway] involved in renal aging. Research in recent years has revealed that several stressors or complications such as rejection after renal transplantation can lead to accelerated renal aging with detrimental effects with the establishment of chronic proinflammatory cellular phenotypes within the kidney. Despite a greater understanding of these mechanisms, the role of complement system in the context of the AKI-to-CKD transition and renal inflammaging is still poorly explored. The purpose of this review is to summarize recent findings describing the role of complement in AKI-to-CKD transition. We will also address how and when complement inhibitors might be used to prevent AKI and CKD progression, therefore improving graft function.
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Activation of complement cascades by DAMPs in APCs releases C3a, C3b, and C5a components.
“Moreover, activation of complement cascades by DAMPs in APCs releases C3a, C3b, and C5a components.”
From Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine (2023) · cites this paper as [44]
The Overview of the Complement System (page not provided) says DAMPs can activate complement cascades that generate C3a, C3b, and C5a. The Immune Cells and Complement System section (page not provided) describes DAMP-induced changes in dendritic cells and local generation of C3a and C5a, but does not establish C3b release specifically in antigen-presenting cells. (LLM, conf=0.87)
Experimental — accuracy not yet measuredC3a and C5a are effective chemoattractants and induce Th1 and Th17 polarization in CD4+ T cells.
“C3a and C5a are effective chemoattractants and induce T helper 1 (Th1) and Th17 polarization in CD4+ T cells [39, 44].”
From Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine (2023) · cites this paper as [44]
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Flagged first, then by citations
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Sorted by citations
Kasravi, M., Ahmadi, A., Babajani, A., Mazloomnejad, R., Hatamnejad, M. R., Shariatzadeh, S., Bahrami, S., & Niknejad, H. (2023) · Biomaterials Research · doi:10.1186/s40824-023-00348-z · Cited by 316 · see citing works
“C3a and C5a are effective chemoattractants and induce T helper 1 (Th1) and Th17 polarization in CD4+ T cells [39, 44].”
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- Authors
- Franzin, R., Stasi, A., Fiorentino, M., Stallone, G., Cantaluppi, V., Gesualdo, L., & Castellano, G.
- Affiliations
- Università degli Studi del Piemonte Orientale “Amedeo Avogadro” (IT)
- University of Bari Aldo Moro (IT)
- University of Foggia (IT)
- Corresponding author
- Franzin, Rossana
- Castellano, Giuseppe
- ORCID
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2020-05-07
- Volume
- 11
- Pages
- 734-734
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC7221190
- OpenAlex
- W3023741319
- Cited by
- 93
- References
- 270
- Citations by year
- 2026: 11 · 2025: 13 · 2024: 13 · 2023: 13 · 2022: 12 · 2021: 22 · 2020: 9
- FWCI
- 1.37
- Type
- journal article
- Language
- en
- Update notices
- corrigendum (2021-01-08)
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion, cc-by)
- Funders
- Universita degli Studi di Bari Aldo Moro
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
- Health Sciences › Medicine › Transplantation › Renal Transplantation Outcomes and Treatments
- Keywords
- inflammaging, complement system, acute kidney injury, chronic kidney disease, AKI-to-CKD transition, delayed graft function, kidney transplantation, kidney aging, complement inhibitors, TGF-beta signaling, Wnt/β-catenin signaling, p16INK4a, graft rejection
- MeSH terms
- Aging, Animals, Complement System Proteins, Complement Activation, Humans, Kidney, Reperfusion Injury, Kidney Transplantation, Disease Progression, Epigenesis, Genetic, Complement Inactivating Agents, Mice, Renal Insufficiency, Chronic, Delayed Graft Function, Acute Kidney Injury
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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