Evidence map›Paper›PMID 28683968›Full record

ReviewJournal of the American College of Cardiology2017

Basic Biology of Oxidative Stress and the Cardiovascular System: Part 1 of a 3-Part Series.

Michael N Sack, Frej Y Fyhrquist, Outi J Saijonmaa, Valentin Fuster, Jason C Kovacic

Abstract readReview
In one paragraph

Review in Journal of the American College of Cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
–field-weighted citation impact
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

114 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Cannabidiol Protects the Neonatal Mouse Heart from Hyperoxia-Induced Injury.International journal of molecular sciences · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. [Advances in hydrogel drug delivery systems for myocardial infarction treatment].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
    Review
  14. Modulation of Redox-Sensitive Cardiac Ion Channels.Antioxidants (Basel, Switzerland) · 2025
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Vessel-On-A-Chip Coupled Proteomics Reveal Pressure-Overload-Induced Vascular Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  20. Article

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

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.

Michael N SackCardiovascular and Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Electronic address: sackm@nih.gov.
Frej Y FyhrquistMinerva Institute for Medical Research, Helsinki, Finland. Electronic address: frej.fyhrquist@helsinki.fi.
Outi J SaijonmaaMinerva Institute for Medical Research, Helsinki, Finland.
Valentin FusterZena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York; Marie-Josée and Henry R. Kravis Cardiovascular Health Center, Icahn School of Medicine at Mount Sinai, New York, New York; Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Jason C KovacicZena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: jason.kovacic@mountsinai.org.

Funding

Mitochondrial Biology in DiseaseZIAHL005102 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SACK, MICHAEL · 2009 to 2025
$22.7M
Toward Therapeutic Manipulation of Endothelial to Mesenchymal TransitionR01HL130423 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ISHIKAWA, KIYOTAKE, KOVACIC, JASON CIRIL · 2016 to 2020
$2.1M
Mitochondrial Biology in Cardiovascular DiseaseZ01HL005102 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SACK, MICHAEL · 2005 to 2008
$1.2M
Intramural NIH HHS Z01 HL005102NHLBI NIH HHS R01 HL130423
6 · The paper itself

Abstract

The generation of reactive oxygen species (ROS) is a fundamental aspect of normal human biology. However, when ROS generation exceeds endogenous antioxidant capacity, oxidative stress arises. If unchecked, ROS production and oxidative stress mediate tissue and cell damage that can spiral in a cycle of inflammation and more oxidative stress. This article is part 1 of a 3-part series covering the role of oxidative stress in cardiovascular disease. The broad theme of this first paper is the mechanisms and biology of oxidative stress. Specifically, the authors review the basic biology of oxidative stress, relevant aspects of mitochondrial function, and stress-related cell death pathways (apoptosis and necrosis) as they relate to the heart and cardiovascular system. They then explore telomere biology and cell senescence. As important regulators and sensors of oxidative stress, telomeres are segments of repetitive nucleotide sequence at each end of a chromosome that protect the chromosome ends from deterioration.

Indexed as

AgingOxidative StressAnimalsApoptosisCardiovascular DiseasesHumansReactive Oxygen SpeciesReactive Oxygen Speciesapoptosismitochondrianecrosisreactive oxygen speciessenescencesirtuintelomere

Identifiers

PMID28683968
PMCPMC5551687

What OpenQuestion holds

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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.