Evidence map›Paper›PMID 36707861›Full record

ArticleJournal of translational medicine2023

Predisposition to cortical neurodegenerative changes in brains of hypertension prone rats.

Moti Ben-Shabat, Yaseen Awad-Igbaria, Shifra Sela, Bella Gross, Yoram Yagil, Chana Yagil, Eilam Palzur

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Animal models of hypertension and concurrent organs injury.Animal models and experimental medicine · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. 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

7 authors at 3 institutions in 1 country.

Moti Ben-Shabat *Research Institute of Galilee Medical Center, Nahariya, Israel.
Yaseen Awad-Igbaria *Research Institute of Galilee Medical Center, Nahariya, Israel.
Shifra SelaResearch Institute of Galilee Medical Center, Nahariya, Israel.
Bella GrossResearch Institute of Galilee Medical Center, Nahariya, Israel.
Yoram YagilLaboratory for Molecular Medicine, Barzilai University Medical Center, Ashkelon, Israel.
Chana YagilLaboratory for Molecular Medicine, Barzilai University Medical Center, Ashkelon, Israel.
Eilam PalzurResearch Institute of Galilee Medical Center, Nahariya, Israel. Eilam.palzur@gmail.com.ORCID 0000-0003-2032-2974
Western Galilee Hospital · ILBar-Ilan University · ILBen-Gurion University of the Negev · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSubstantial evidence suggests that hypertension is a significant risk factor for cognitive decline. However, it is unclear whether the genetic predisposition to hypertension is also associated with cellular dysfunction that promotes neurodegeneration.

methodsChanges in blood pressure were evaluated following dietary salt-loading or administration of a regular diet in Sabra Normotensive (SBN/y) and Sabra Hypertension-prone rats (SBH/y). We performed quantitative RT-PCR and immunofluorescence staining in brain cortical tissues before salt loading and 6 and 9 months after salt loading. To examine the expression of brain cortical proteins involved in the gene regulation (Histone Deacetylase-HDAC2; Histone Acetyltransferase 1-HAT1), stress response (Activating Transcription Factor 4-ATF4; Eukaryotic Initiation Factor 2- eIF2α), autophagy (Autophagy related 4A cysteine peptidase- Atg4a; light-chain 3-LC3A/B; mammalian target of rapamycin complex 1- mTORC1) and apoptosis (caspase-3).

resultsPrior to salt loading, SBH/y compared to SBN/y expressed a significantly higher level of cortical HAT1 (protein), Caspase-3 (mRNA/protein), LC3A, and ATF4 (mRNA), lower levels of ATG4A (mRNA/protein), LC3A/B, HDAC2 (protein), as well as a lower density of cortical neurons. Following dietary salt loading, SBH/y but not SBN/y developed high blood pressure. In hypertensive SBH/y, there was significant upregulation of cortical HAT1 (protein), Caspase-3 (protein), and eIF2α ~ P (protein) and downregulation of HDAC2 (protein) and mTORC1 (mRNA), and cortical neuronal loss.

conclusionsThe present findings suggest that genetic predisposition to hypertension is associated in the brain cortex with disruption in autophagy, gene regulation, an abnormal response to cellular stress, and a high level of cortical apoptosis, and could therefore exacerbate cellular dysfunction and thereby promote neurodegeneration.

Indexed as

HypertensionSodium Chloride, DietaryAnimalsBrainCaspase 3Genetic Predisposition to DiseaseMammalsRatsRNA, MessengerSodium ChlorideCaspase 3RNA, MessengerSodium ChlorideSodium Chloride, DietaryDietary Salt LoadingGenetic predispositionHypertensionNeurodegenerationSBH/ySBN/y

Identifiers

PMID36707861
PMCPMC9881299
OpenAlexW4318215173

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.