Evidence map›Paper›PMID 41221587›Full record

ArticleHypertension (Dallas, Tex. : 1979)2026

Temporal Proteomic Remodeling of Cerebral Arteries in Male Hypertensive Rats.

Joakim A Bastrup, Catarina Rippe, Karl Swärd, Thomas A Jepps

Abstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Joakim A BastrupVascular Biology Group, Department of Biomedical Sciences, University of Copenhagen, Denmark (J.A.B., T.A.J.).ORCID 0000-0002-4292-5234
Catarina RippeCellular Biomechanics, Department of Experimental Medical Science, Lund University, Sweden (C.R., K.S.).ORCID 0000-0001-8621-9836
Karl SwärdCellular Biomechanics, Department of Experimental Medical Science, Lund University, Sweden (C.R., K.S.).ORCID 0000-0002-7255-5510
Thomas A JeppsVascular Biology Group, Department of Biomedical Sciences, University of Copenhagen, Denmark (J.A.B., T.A.J.).ORCID 0000-0002-9903-714X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypertension is a significant risk factor for several neurological disorders, including stroke and dementia, yet the molecular mechanisms underlying these risks remain poorly understood. In this study, we investigated temporal proteomic remodeling of the cerebrovasculature in male spontaneously hypertensive rats and normotensive Wistar-Kyoto controls at 30 and 40 weeks of age, representing the effect of untreated hypertension from early adulthood to midlife.

methodsUsing male 30- and 40-week-old spontaneously hypertensive rats and Wistar-Kyoto rats, we have performed discovery-based proteomics, histological imaging, and RNA-sequencing data analysis.

resultsProteomic analysis displayed a significant age-dependent change in the protein composition of the cerebrovasculature in the spontaneously hypertensive rat model, which is partly mediated via reduced SRF (serum response factor) expression and associated regulon. Pathway analysis revealed a transient upregulation of mitotic (M-phase) proteins at 30 weeks, indicative of maladaptive smooth muscle proliferation. By 40 weeks, the expression of these proteins was normalized; however, ECM (extracellular matrix)-associated proteins diverged substantially. The ECM remodeling was supported by increased media-to-circumference ratio and collagen deposition from histological analysis.

conclusionsOur findings demonstrate that hypertension drives a temporal shift in cerebrovascular remodeling, transitioning from early maladaptive smooth muscle proliferation to later ECM-driven structural changes. This progression suggests that the pathogenic mechanisms underlying hypertensive vascular injury are dynamic across the life course, with distinct phases that may require different and timely therapeutic approaches to mitigate the risks of neurovascular diseases.

Indexed as

Cerebral ArteriesHypertensionProteomicsVascular RemodelingAnimalsDisease Models, AnimalExtracellular MatrixMaleRatsRats, Inbred SHRRats, Inbred WKYagingbrain diseasescerebral arterieshypertensionproteomics

Identifiers

PMID41221587
PMCPMC12711280

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.