Evidence map›Paper›PMID 25432896›Full record

ReviewCurrent hypertension reports2015

Hypertension and insulin resistance: implications of mitochondrial dysfunction.

Walter Manucha, Bob Ritchie, León Ferder

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hypertension reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.1field-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

28 citing papers in PubMed, 44 citations in OpenAlex.

  1. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  2. Article
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  4. Sodium-glucose cotransporter-2 inhibitors protect tissuesWorld journal of experimental medicine · 2024
    Review
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  6. Article
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  11. Article
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  17. The emerging role of sorting nexins in cardiovascular diseases.Clinical science (London, England : 1979) · 2019
    Review
  18. Article
  19. Article
  20. Melatonin, mitochondria and hypertension.Cellular and molecular life sciences : CMLS · 2017
    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

3 authors at 2 institutions in 2 countries.

Walter ManuchaÁrea de Farmacología, Departamento de Patología, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo Centro Universitario, Mendoza, 5500, Argentina, wmanucha@yahoo.com.ar.
Bob Ritchie
León Ferder
Ponce Health Sciences University · PRUniversidad Nacional de Cuyo · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are the primary generators of cellular reactive oxygen species (ROS); their pathophysiological roles in hypertension and insulin resistance are but imperfectly understood. Mitochondrial dysfunction has been linked to the etiologies of many complex diseases, but many other factors, including the upregulation of the renin-angiotensin system (RAS) and vitamin D deficiency, have also been implicated in hypertension pathogenesis. Hypertension resulting from the disruption of the RAS contributes to the risk of cardiovascular disease. Likewise, experimental and clinical evidence indicate that RAS stimulation and low vitamin D levels are inversely related and represent risk factors associated with the pathogenesis of hypertension. Furthermore, RAS activation induces insulin resistance, resulting in increases in ROS levels. High levels of ROS are harmful to cells, having the potential to trigger both mitochondrial-mediated apoptosis and the degradation of the mitochondrial DNA. Diabetes risk is also associated with high levels of oxidative stress; taking vitamin D, however, may reduce that risk. The finding that mitochondria possess both a functional RAS and vitamin D receptors is the starting point for improving our understanding of the interaction of mitochondria and chronic disease states, which understanding should lead to decreases in the chronic disease burden attributable to hypertension, diabetes, or both.

Indexed as

Insulin ResistanceHumansHypertensionMitochondriaOxidative Stress

Identifiers

PMID25432896
OpenAlexW2028128978

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.