Evidence map›Paper›PMID 25385092›Full record

ReviewEuropean heart journal2014

Mitochondrial injury and dysfunction in hypertension-induced cardiac damage.

Alfonso Eirin, Amir Lerman, Lilach O Lerman

Open access · bronzeAbstract readReview
In one paragraph

Review in European heart journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Gout and NLRP3 Inflammasome Biology.Arthritis & rheumatology (Hoboken, N.J.) · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
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  13. Review
  14. Article
  15. Article
  16. Article
  17. Anthracycline-induced hypertension in pediatric cancer survivors: unveiling the long-term cardiovascular risks.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024
    Review
  18. Article
  19. Article
  20. Article

3 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

3 authors at 1 institution in 1 country.

Alfonso EirinDivision of Nephrology and Hypertension, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
Amir LermanCardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
Lilach O LermanDivision of Nephrology and Hypertension, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA lerman.lilach@mayo.edu.
WinnMed · US

Funding

CT imaging for the assessment of kidney injury distal to renal artery stenosisR01DK073608 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2006 to 2015
$3.1M
Hypoxia and inflammatory injury in human renovascular hypertensionR01DK100081 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O, TEXTOR, STEPHEN C · 2014 to 2018
$2.8M
Role of Endothelial Progenitor Cells in vascular Aging and CalcificationR01AG031750 · NIA · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP, LERMAN, AMIR · 2010 to 2014
$2.0M
Low-Energy Shockwave Treatment Distal To Peripheral Vascular DiseaseR21HL121561 · NHLBI · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2014 to 2015
$434k
NHLBI NIH HHS HL-121561NIA NIH HHS AG31750NIDDK NIH HHS DK100081NIDDK NIH HHS DK73608NIDDK NIH HHS R01 DK073608
6 · The paper itself

Abstract

Hypertension remains an important modifiable risk factor for cardiovascular disease, associated with increased morbidity and mortality. Deciphering the mechanisms involved in the pathogenesis of hypertension is critical, as its prevalence continues increasing worldwide. Mitochondria, the primary cellular energy producers, are numerous in parenchymal cells of the heart, kidney, and brain, major target organs in hypertension. These membrane-bound organelles not only maintain cellular respiration but also modulate several functions of the cell including proliferation, apoptosis, generation of reactive oxygen species, and intracellular calcium homeostasis. Therefore, mitochondrial damage and dysfunction compromise overall cell functioning. In recent years, significant advances increased our understanding of mitochondrial morphology, bioenergetics, and homeostasis, and in turn of their role in several diseases, so that mitochondrial abnormalities and dysfunction have been identified in experimental models of hypertension. In this review, we summarize current knowledge of the contribution of dysfunctional mitochondria to the pathophysiology of hypertension-induced cardiac damage, as well as available evidence of mitochondrial injury-induced damage in other organs. Finally, we discuss the capability of antihypertensive therapy to ameliorate hypertensive mitochondrial injury, and the potential position of mitochondria as therapeutic targets in patients with hypertension.

Indexed as

AnimalsAntihypertensive AgentsDisease Models, AnimalHeart DiseasesHomeostasisHumansHypertensionMiceMitochondria, HeartMitochondrial DiseasesRatsReactive Oxygen SpeciesSwineAntihypertensive AgentsReactive Oxygen SpeciesBlood pressureHypertensionMitochondria

Identifiers

PMID25385092
PMCPMC4258226
OpenAlexW2014901923

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.