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Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension
Faraco G, Sugiyama Y, Lane D, Garcia-Bonilla L, Chang H, Santisteban MM, Racchumi G, Murphy M et al.. The Journal of clinical investigation, 2016-11-14
Topic: Brain proteins, microglia and lab models
Hypertension is a leading risk factor for dementia, but the mechanisms underlying its damaging effects on the brain are poorly understood. Due to a lack of energy reserves, the brain relies on continuous delivery of blood flow to its active regions in accordance with their dynamic metabolic needs. Hypertension disrupts these vital regulatory mechanisms, leading to the neuronal dysfunction and damage underlying cognitive impairment. Elucidating the cellular bases of these impairments is essential for developing new therapies. Perivascular macrophages (PVMs) represent a distinct population of resident brain macrophages that serves key homeostatic roles but also has the potential to generate large amounts of reactive oxygen species (ROS). Here, we report that PVMs are critical in driving the alterations in neurovascular regulation and attendant cognitive impairment in mouse models of hypertension. This effect was mediated by an increase in blood-brain barrier permeability that allowed angiotensin II to enter the perivascular space and activate angiotensin type 1 receptors in PVMs, leading to production of ROS through the superoxide-producing enzyme NOX2. These findings unveil a pathogenic role of PVMs in the neurovascular and cognitive dysfunction associated with hypertension and identify these cells as a putative therapeutic target for diseases associated with cerebrovascular oxidative stress.
Key findings
- These findings unveil a pathogenic role of PVMs in the neurovascular and cognitive dysfunction associated with hypertension and identify these cells as a putative therapeutic target for diseases associated with cerebrovascular oxidative stress.
Why it matters
In mouse models of hypertension, perivascular macrophages drove blood vessel and cognitive problems through a pathway involving angiotensin II, angiotensin type 1 receptors and the enzyme NOX2. The authors propose these cells as a possible therapeutic target, but this is animal research and no treatment is proven.
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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 | 1 / 5 | 2016 — within 20 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 | 6 / 7 | Cited 350 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 29.2 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 4 / 6 | Cited 12.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 13 other studies in this library |
| Still being cited | 3 / 4 | Cited 118 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Costantino Iadecola: h-index 128 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Weill Cornell Medicine: institution h-index 1,163 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 27841763) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 51 / 100 | — |
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Read the original
- DOI: 10.1172/jci86950
- PubMed: 27841763
- 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. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
APA 7th
Faraco, G., Sugiyama, Y., Lane, D., Garcia-Bonilla, L., Chang, H., Santisteban, M. M., et al. (2016). Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension. The Journal of clinical investigation. https://doi.org/10.1172/jci86950
Vancouver
Faraco G, Sugiyama Y, Lane D, Garcia-Bonilla L, Chang H, Santisteban MM, et al. Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension. The Journal of clinical investigation. 2016. doi:10.1172/jci86950. PMID: 27841763.
BibTeX
@article{faraco2016-27841763,
author = {Faraco, G. and Sugiyama, Y. and Lane, D. and Garcia-Bonilla, L. and Chang, H. and Santisteban, M. M. and Racchumi, G. and Murphy, M. and others},
title = {{Perivascular macrophages mediate the neurovascular and cognitive dysfunction associated with hypertension}},
journal = {The Journal of clinical investigation},
year = {2016},
doi = {10.1172/jci86950},
pmid = {27841763},
url = {https://doi.org/10.1172/jci86950}
}
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