Evidence map›Paper›PMID 21546574›Full record

ArticleJournal of the American Society of Nephrology : JASN2011

Mitochondria-targeted peptide accelerates ATP recovery and reduces ischemic kidney injury.

Hazel H Szeto, Shaoyi Liu, Yi Soong, Dunli Wu, Shaun F Darrah, Feng-Ying Cheng, Zhihong Zhao, Michael Ganger, Clara Y Tow, Surya V Seshan

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 papers.

0numbers the graph read from it
0cells of the map it votes in
190citing papers in PubMed
12.5field-weighted citation impact, top 1% 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

190 citing papers in PubMed, 306 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Trial
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Microvascular Health as a Key Determinant of Organismal Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  14. Review
  15. Article
  16. Review
  17. Therapies for Mitochondrial Disease: Past, Present, and Future.Journal of inherited metabolic disease · 2025
    Review
  18. Article
  19. Article
  20. Article

130 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Hazel H SzetoDepartment of Pharmacology, Weill Cornell Medical College, New York, NY 10021, USA. hhszeto@med.cornell.edu
Shaoyi Liu
Yi Soong
Dunli Wu
Shaun F Darrah
Feng-Ying Cheng
Zhihong Zhao
Michael Ganger
Clara Y Tow
Surya V Seshan
Cornell University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The burst of reactive oxygen species (ROS) during reperfusion of ischemic tissues can trigger the opening of the mitochondrial permeability transition (MPT) pore, resulting in mitochondrial depolarization, decreased ATP synthesis, and increased ROS production. Rapid recovery of ATP upon reperfusion is essential for survival of tubular cells, and inhibition of oxidative damage can limit inflammation. SS-31 is a mitochondria-targeted tetrapeptide that can scavenge mitochondrial ROS and inhibit MPT, suggesting that it may protect against ischemic renal injury. Here, in a rat model of ischemia-reperfusion (IR) injury, treatment with SS-31 protected mitochondrial structure and respiration during early reperfusion, accelerated recovery of ATP, reduced apoptosis and necrosis of tubular cells, and abrogated tubular dysfunction. In addition, SS-31 reduced medullary vascular congestion, decreased IR-mediated oxidative stress and the inflammatory response, and accelerated the proliferation of surviving tubular cells as early as 1 day after reperfusion. In summary, these results support MPT as an upstream target for pharmacologic intervention in IR injury and support early protection of mitochondrial function as a therapeutic maneuver to prevent tubular apoptosis and necrosis, reduce oxidative stress, and reduce inflammation. SS-31 holds promise for the prevention and treatment of acute kidney injury.

Indexed as

Acute Kidney InjuryAdenosine TriphosphateAnimalsAntioxidantsApoptosisKidney TubulesMaleMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreModels, AnimalOligopeptidesOxidative StressRatsRats, Sprague-DawleyReactive Oxygen SpeciesAdenosine TriphosphateAntioxidantsarginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamideMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreOligopeptidesReactive Oxygen Species

Identifiers

PMID21546574
PMCPMC3103724
OpenAlexW2159285342

What OpenQuestion holds

Textmetadata
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.