Evidence map›Paper›PMID 27876411›Full record

ReviewPharmacological research2017

Disruption of mitochondrial quality control in peripheral artery disease: New therapeutic opportunities.

Cintia B Ueta, Katia S Gomes, Márcio A Ribeiro, Daria Mochly-Rosen, Julio C B Ferreira

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacological research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.5field-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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. The Aging Gut-Brain Axis: Effects of Dietary Polyphenols and Metal Exposure.Chronic diseases and translational medicine · 2025
    Review
  3. Article
  4. Article
  5. Ischemia-Reperfusion Injury in Peripheral Artery Disease and Traditional Chinese Medicine Treatment.Evidence-based complementary and alternative medicine : eCAM · 2021
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Resveratrol and Brain Mitochondria: a Review.Molecular neurobiology · 2018
    Review
  11. Review
  12. 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

5 authors at 2 institutions in 2 countries.

Cintia B UetaDepartment of Anatomy, Institute of Biomedical Sciences, University of São Paulo, Brazil.
Katia S GomesDepartment of Anatomy, Institute of Biomedical Sciences, University of São Paulo, Brazil.
Márcio A RibeiroDepartment of Anatomy, Institute of Biomedical Sciences, University of São Paulo, Brazil.
Daria Mochly-RosenDepartment of Chemical and Systems Biology, Stanford University School of Medicine, USA.
Julio C B FerreiraDepartment of Anatomy, Institute of Biomedical Sciences, University of São Paulo, Brazil. Electronic address: jcesarbf@usp.br.
Universidade de São Paulo · BRStanford University · US

Funding

Protein Kinase C Isozymes in Ischemic HeartR01HL052141 · NHLBI · STANFORD UNIVERSITY · PI MOCHLY-ROSEN, DARIA · 1996 to 2021
$8.5M
MECHANISMS OF ETHANOL-INDUCED CARDIAC PROTECTIONR01AA011147 · NIAAA · STANFORD UNIVERSITY · PI DARIA MOCHLY-ROSEN · 1996 to 2026
$8.2M
Mechanisms of Ethanol-Induced Cardiac ProtectionR37AA011147 · NIAAA · STANFORD UNIVERSITY · PI MOCHLY-ROSEN, DARIA · 2009 to 2018
$5.3M
NHLBI NIH HHS R01 HL052141NIAAA NIH HHS R01 AA011147NIAAA NIH HHS R37 AA011147
6 · The paper itself

Abstract

Peripheral artery disease (PAD) is a multifactorial disease initially triggered by reduced blood supply to the lower extremities due to atherosclerotic obstructions. It is considered a major public health problem worldwide, affecting over 200 million people. Management of PAD includes smoking cessation, exercise, statin therapy, antiplatelet therapy, antihypertensive therapy and surgical intervention. Although these pharmacological and non-pharmacological interventions usually increases blood flow to the ischemic limb, morbidity and mortality associated with PAD continue to increase. This scenario raises new fundamental questions regarding the contribution of intrinsic metabolic changes in the distal affected skeletal muscle to the progression of PAD. Recent evidence suggests that disruption of skeletal muscle mitochondrial quality control triggered by intermittent ischemia-reperfusion injury is associated with increased morbidity in individuals with PAD. The mitochondrial quality control machinery relies on surveillance systems that help maintaining mitochondrial homeostasis upon stress. In this review, we describe some of the most critical mechanisms responsible for the impaired skeletal muscle mitochondrial quality control in PAD. We also discuss recent findings on the central role of mitochondrial bioenergetics and quality control mechanisms including mitochondrial fusion-fission balance, turnover, oxidative stress and aldehyde metabolism in the pathophysiology of PAD, and highlight their potential as therapeutic targets.

Indexed as

AnimalsEnergy MetabolismHumansMitochondriaMuscle, SkeletalOxidative StressPeripheral Arterial DiseasePharmaceutical PreparationsReperfusion InjuryPharmaceutical Preparations4-HydroxynonenalMitochondrial dynamicsMitochondrial metabolismMitophagyMyocyteRedox balance

Identifiers

PMID27876411
PMCPMC5205542
OpenAlexW2552063923

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.