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Endothelial C3a receptor mediates vascular inflammation and blood-brain barrier permeability during aging
Propson NE, Roy ER, Litvinchuk A, Köhl J, Zheng H.. The Journal of clinical investigation, 2021-01-01
Topic: Brain proteins, microglia and lab models
Dysfunction of immune and vascular systems has been implicated in aging and Alzheimer disease; however, their interrelatedness remains poorly understood. The complement pathway is a well-established regulator of innate immunity in the brain. Here, we report robust age-dependent increases in vascular inflammation, peripheral lymphocyte infiltration, and blood-brain barrier (BBB) permeability.
Key findings
- The complement pathway is a well-established regulator of innate immunity in the brain.
- Here, we report robust age-dependent increases in vascular inflammation, peripheral lymphocyte infiltration, and blood-brain barrier (BBB) permeability.
- These phenotypes were subdued by global inactivation and by endothelial cell-specific ablation of C3ar1.
- Using an in vitro model of the BBB, we identified intracellular Ca2+ as a downstream effector of C3a/C3aR signaling and a functional mediator of vascular endothelial cadherin junction and barrier integrity.
Why it matters
In this work, age-dependent vascular inflammation, lymphocyte infiltration and blood-brain barrier permeability were reduced by inactivating the C3a receptor, and intracellular calcium was identified as a downstream mediator in an in vitro blood-brain barrier model. It is early laboratory work and does not show a treatment, cure or prevention for Alzheimer's disease.
Study details
- Evidence strengthLow
How this study scored 51/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (The Journal of clinical investigation) |
| Journal's citation record | 4 / 4 | Journal of Clinical Investigation: journal h-index 706 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 3 / 5 | 2021 — within 6 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 256 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 36.6 citations a year over 7 year(s) since 2021 |
| Impact for its field and year | 4 / 6 | Cited 8.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 6 other studies in this library |
| Still being cited | 3 / 4 | Cited 154 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Hui Zheng: h-index 77 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Baylor College of Medicine: institution h-index 1,607 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 32990682) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 51 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1172/jci140966
- PubMed: 32990682
- Original source →
- Free full text: Journal of Clinical Investigation →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Propson, N. E., Roy, E. R., Litvinchuk, A., Köhl, J., & Zheng, H. (2021). Endothelial C3a receptor mediates vascular inflammation and blood-brain barrier permeability during aging. The Journal of clinical investigation. https://doi.org/10.1172/jci140966
Vancouver
Propson NE, Roy ER, Litvinchuk A, Köhl J, Zheng H. Endothelial C3a receptor mediates vascular inflammation and blood-brain barrier permeability during aging. The Journal of clinical investigation. 2021. doi:10.1172/jci140966. PMID: 32990682.
BibTeX
@article{propson2021-32990682,
author = {Propson, N. E. and Roy, E. R. and Litvinchuk, A. and Köhl, J. and Zheng, H.},
title = {{Endothelial C3a receptor mediates vascular inflammation and blood-brain barrier permeability during aging}},
journal = {The Journal of clinical investigation},
year = {2021},
doi = {10.1172/jci140966},
pmid = {32990682},
url = {https://doi.org/10.1172/jci140966}
}
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