Evidence map›Paper›PMID 24043248›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2013

Role of mitochondrial oxidative stress in hypertension.

Sergey I Dikalov, Zoltan Ungvari

Abstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing 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

106 citing papers in PubMed.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Mitochondrial Dysfunction in Cardiovascular Diseases.International journal of molecular sciences · 2025
    Review
  12. Endothelial Function Biomarkers in Hypertension.Current medicinal chemistry · 2025
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

46 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

2 authors.

Sergey I DikalovDivision of Clinical Pharmacology, Free Radicals in Medicine Core, Vanderbilt University Medical Center, Nashville, Tennessee; and.
Zoltan Ungvari

Funding

Effects of Radiation on Brain Microvasculature and CognitionR01NS056218 · NINDS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CSISZAR, ANNA, SONNTAG, WILLIAM EDMUND · 2007 to 2018
$3.6M
Role of SIRT1 in vasoprotectionR01AT006526 · NCCIH · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI UNGVARI, ZOLTAN ISTVAN · 2010 to 2014
$1.8M
Mitochondrial Oxidative Stress In Angiotensis II Induced Endothelial DysfunctionR01HL094469 · NHLBI · VANDERBILT UNIVERSITY · PI DIKALOV, SERGEY · 2010 to 2013
$1.6M
NCCIH NIH HHS AT-006526NCCIH NIH HHS R01 AT006526NHLBI NIH HHS HL-094469NHLBI NIH HHS R01 HL094469NINDS NIH HHS R01 NS056218
6 · The paper itself

Abstract

Based on mosaic theory, hypertension is a multifactorial disorder that develops because of genetic, environmental, anatomical, adaptive neural, endocrine, humoral, and hemodynamic factors. It has been recently proposed that oxidative stress may contribute to all of these factors and production of reactive oxygen species (ROS) play an important role in the development of hypertension. Previous studies focusing on the role of vascular NADPH oxidases provided strong support of this concept. Although mitochondria represent one of the most significant sources of cellular ROS generation, the regulation of mitochondrial ROS generation in the cardiovascular system and its pathophysiological role in hypertension are much less understood. In this review, the role of mitochondrial oxidative stress in the pathophysiology of hypertension and cross talk between angiotensin II signaling, pathways involved in mechanotransduction, NADPH oxidases, and mitochondria-derived ROS are considered. The possible benefits of therapeutic strategies that have the potential to attenuate mitochondrial oxidative stress for the prevention/treatment of hypertension are also discussed.

Indexed as

Blood PressureOxidative StressAngiotensin IIAnimalsAntihypertensive AgentsAntioxidantsCardiovascular SystemHumansHypertensionMechanotransduction, CellularMitochondriaNADPH OxidasesReactive Oxygen SpeciesRenin-Angiotensin SystemRisk FactorsAngiotensin IIAntihypertensive AgentsAntioxidantsNADPH OxidasesReactive Oxygen Speciesantioxidanthypertensionmitochondriaoxidative stresssuperoxide

Identifiers

PMID24043248
PMCPMC3840266

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.