Evidence map›Paper›PMID 29714040›Full record

ArticleExperimental physiology2018

Mitoprotection preserves the renal vasculature in porcine metabolic syndrome.

Alfonso Eirin, Ahmad F Hedayat, Christopher M Ferguson, Stephen C Textor, Amir Lerman, Lilach O Lerman

Open access · bronzeAbstract read
In one paragraph

Article in Experimental physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Trial
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  5. Article
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  7. Article
  8. SS-31, a Mitochondria-Targeting Peptide, Ameliorates Kidney Disease.Oxidative medicine and cellular longevity · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Renovascular disease induces mitochondrial damage in swine scattered tubular cells.American journal of physiology. Renal physiology · 2019
    Article
  15. Enhancing Mitochondrial Health to Treat Hypertension.Current hypertension reports · 2018
    Review
  16. Review
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

6 authors at 1 institution in 1 country.

Alfonso EirinDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
Ahmad F HedayatDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
Christopher M FergusonDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
Stephen C TextorDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
Amir LermanCardiovascular Diseases, Mayo Clinic, Rochester, MN, USA.
Lilach O LermanDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.ORCID 0000-0002-3271-3887
Mayo Clinic · US

Funding

Ultrasound Shockwave Therapy for Post-Stenotic Microvascular RemodelingR01HL123160 · NHLBI · MAYO CLINIC ROCHESTER · PI LERMAN, AMIR, LERMAN, LILACH O · 2015 to 2018
$3.0M
Hypoxia and inflammatory injury in human renovascular hypertensionR01DK100081 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O, TEXTOR, STEPHEN C · 2014 to 2018
$2.8M
MSC-derived microvesicles in metabolic syndrome and renovascular diseaseR01DK102325 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2015 to 2018
$2.8M
Noninvasive assessment of renal fibrosis using magnetization transfer MRIU01DK104273 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2014 to 2018
$1.8M
A potential role for mitoprotection in preserving the kidney in metabolic syndrome and renal artery stenosisK08DK106427 · NIDDK · MAYO CLINIC ROCHESTER · PI EIRIN, ALFONSO · 2015 to 2019
$819k
NHLBI NIH HHS R01 HL123160NIDDK NIH HHS K08 DK106427NIDDK NIH HHS R01 DK100081NIDDK NIH HHS R01 DK102325NIDDK NIH HHS U01 DK104273
6 · The paper itself

Abstract

NEW

findingsWhat is the central question of this study? We hypothesized that chronic mitoprotection would decrease renal vascular remodelling and dysfunction in swine metabolic syndrome. What is the main finding and its importance? This study shows that experimental metabolic syndrome exerts renal microvascular and endothelial cell mitochondrial injury, which were attenuated by mitoprotection, underscoring the contribution of mitochondrial injury to the pathogenesis of metabolic syndrome-induced vascular damage. ABSTRACT: The metabolic syndrome (MetS) induces intrarenal microvascular disease, which may involve mitochondrial injury. The mitochondrial cardiolipin-targeting peptide elamipretide (ELAM) improves the microcirculation in post-stenotic kidneys, but its ability to attenuate MetS-induced renal vascular damage is unknown. We hypothesized that chronic treatment with ELAM would decrease renal vascular remodelling and function in swine MetS. Pigs were studied after 16 weeks of diet-induced MetS, MetS treated for the last 4 weeks with daily injections of ELAM (0.1 mg kg

Indexed as

AnimalsAntioxidantsApoptosisEndothelial CellsFemaleGlomerular Filtration RateKidneyMetabolic SyndromeMitochondriaOligopeptidesOxidative StressRenal CirculationSwineAntioxidantsarginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamideOligopeptidescardiolipinkidneymetabolic syndromemicrovascularmitochondria

Identifiers

PMID29714040
PMCPMC6026037
OpenAlexW2800989504

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.