Evidence map›Paper›PMID 24048008›Full record

ArticleJournal of hypertension2014

Mitochondrial targeted peptides attenuate residual myocardial damage after reversal of experimental renovascular hypertension.

Alfonso Eirin, Barbara J Williams, Behzad Ebrahimi, Xin Zhang, John A Crane, Amir Lerman, Stephen C Textor, Lilach O Lerman

Open access · greenAbstract read
In one paragraph

Article in Journal of hypertension, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Mitophagy in hypertension-mediated organ damage.Frontiers in cardiovascular medicine · 2023
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Novel therapeutic strategies for renovascular disease.Current opinion in nephrology and hypertension · 2019
    Review
  16. Review
  17. Enhancing Mitochondrial Health to Treat Hypertension.Current hypertension reports · 2018
    Review
  18. Article
  19. Article
  20. 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

8 authors at 2 institutions in 1 country.

Alfonso EirinaDivision of Nephrology and Hypertension, Department of Internal Medicine bDivision of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA.
Barbara J Williams
Behzad Ebrahimi
Xin Zhang
John A Crane
Amir Lerman
Stephen C Textor
Lilach O Lerman
Hypertension Institute · USMayo Clinic · US

Funding

CT Evaluation of the Myocardial Effects of Risk FactorsR01HL077131 · NHLBI · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2004 to 2013
$2.8M
Institutional Short-Term Research Training for Students of DiversityR25HL092621 · NHLBI · MAYO CLINIC ROCHESTER · PI HORAZDOVSKY, BRUCE F · 2008 to 2023
$2.0M
NHLBI NIH HHS HL77131NHLBI NIH HHS R01 HL077131NHLBI NIH HHS R25 HL092621
6 · The paper itself

Abstract

backgroundRenovascular hypertension (RVHT) increases cardiovascular morbidity and mortality. Renal revascularization with percutaneous transluminal renal angioplasty and stenting (PTRS) may reverse RVHT but may not fully regress cardiac remodeling and damage, possibly due to persistent myocardial insults. Bendavia is a mitochondrial targeted peptide that reduces ischemic cardiomyopathy by improving mitochondrial function. However, its potential for attenuating residual myocardial damage after reversal of RVHT has not been explored. We hypothesized that treatment with Bendavia as an adjunct to PTRS would improve cardiac function and oxygenation, and decrease myocardial injury in swine RVHT. METHODS AND

resultsAfter 6 weeks of RVHT (unilateral renal artery stenosis) or control, pigs underwent PTRS (or sham), with adjunct continuous infusion of Bendavia (0.05  mg/kg intravenously, 30  min before to 3.5  h after PTRS) or vehicle (n = 7 each). Four weeks later, systolic and diastolic function were assessed by multidetector computed tomography, myocardial oxygenation by blood oxygen level-dependent MRI, and myocardial morphology, apoptosis, mitochondrial biogenesis, and fibrosis evaluated ex vivo. PTRS restored blood pressure in both groups, yet E/A ratio remained decreased. Myocardial oxygenation and mitochondrial biogenesis improved, and myocardial inflammation, oxidative stress, and fibrosis normalized in association with improvement in diastolic function in RVHT + PTRS + Bendavia animals.

conclusionAdjunct Bendavia during PTRS in swine RVHT improved diastolic function and oxygenation and reversed myocardial tissue damage. This approach may allow a novel strategy for preservation of cardiac function and structure in RVHT.

Indexed as

AngioplastyAnimalsApoptosisCardiomyopathiesCollagenFemaleFibrosisHeart Function TestsHypertension, RenovascularKidney Function TestsMicrovesselsMitochondria, HeartOxidative StressOxygenPeptidesSwineCollagenOxygenPeptides

Identifiers

PMID24048008
PMCPMC3976567
OpenAlexW2024271266

What OpenQuestion holds

Textmetadata
LicenceTDM
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.