Evidence map›Paper›PMID 22581415›Full record

ReviewCurrent hypertension reports2012

Oxidative stress in the cardiorenal metabolic syndrome.

Adam Whaley-Connell, James R Sowers

Abstract readReview
In one paragraph

Review in Current hypertension reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

37 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Eplerenone improves kidney function and cardiac performance in obese male mice.Diabetic medicine : a journal of the British Diabetic Association · 2026
    Article
  6. Observational
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Endothelial Dysfunction in Obesity and Therapeutic Targets.Advances in experimental medicine and biology · 2024
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Cellular apoptosis in the cardiorenal axis.Heart failure reviews · 2016
    Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Adam Whaley-ConnellDiabetes and Cardiovascular Center, Harry S Truman VA Medical Center and the University of Missouri-Columbia School of Medicine, Columbia, MO 65213, USA. whaleyconnella@health.missouri.edu
James R Sowers
Harry S. Truman Memorial Veterans' Hospital · US

Funding

ANG II OPPOSES INS MEDIATED VASORELAXATION &GLU UTILZAR01HL073101 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI SOWERS, JAMES RUSSELL · 2004 to 2013
$2.7M
Ang II and Overnutrition and Insulin resistance in Cardiovascular TissueR01HL107910 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI SOWERS, JAMES RUSSELL · 2011 to 2015
$1.8M
NHLBI NIH HHS R01 HL073101NHLBI NIH HHS R01 HL107910
6 · The paper itself

Abstract

Excess visceral adiposity contributes to inappropriate activation of the renin-angiotensin-aldosterone system despite a state of volume expansion and of salt retention that contributes to subclinical elevations of pro-oxidant mechanisms. These adverse effects are mediated by excess generation of reactive oxygen species (ROS) and diminished antioxidant defense mechanisms. Excess tissue (i.e., skeletal muscle, liver, heart) free oxygen radicals contribute to impairments in the insulin-dependent metabolic signaling pathways that regulate glucose utilization/disposal and systemic insulin sensitivity. The generation of ROS is required for normal cell signaling and physiological responses. It is a loss of redox homeostasis that results in a proinflammatory/profibrotic milieu that promotes impairments in insulin metabolic signaling, reduced endothelial-mediated vasorelaxation, and associated cardiovascular and renal structural and functional abnormalities. These maladaptive processes are increasingly recognized as important in the progression of hypertension in the cardiorenal metabolic phenotype. There is increasing evidence to support a critical role for Ang II signaling through the AT(1)R and aldosterone actions through the MR in conjunction with an altered redox-mediating impaired endothelial, cardiac and renal function in this metabolic phenotype. There are emerging clinical data that indicate that therapies that target the renin angiotensin-aldosterone system (RAAS) also attenuate oxidative stress, and improve endothelial, cardiac and renal functions, which collectively contribute to reductions in hypertension.

Indexed as

Insulin ResistanceOxidative StressBlood PressureCardio-Renal SyndromeHumansHypertensionNADPH OxidasesObesityReactive Oxygen SpeciesRenin-Angiotensin SystemRisk FactorsNADPH OxidasesReactive Oxygen Species

Identifiers

PMID22581415
PMCPMC3636553
OpenAlexW2040273911

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.