Evidence mapPaperPMID 41155389Full record

ReviewInternational journal of molecular sciences2025

Endothelial Dysfunction as the Common Pathway Linking Obesity, Hypertension and Atherosclerosis.

Ewelina Młynarska, Kinga Bojdo, Hanna Frankenstein, Katarzyna Krawiranda, Natalia Kustosik, Wiktoria Lisińska, Jacek Rysz, Beata Franczyk

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Article
  4. Covert macrovascular disease and early outcome after ischemic cerebrovascular events.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
    Observational
  5. Review
  6. Article
  7. Review
  8. Observational
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Obesity and Heart Failure: Introducing the Theme.Journal of cardiovascular development and disease · 2026
    Review
  19. Observational
  20. Article
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

8 authors.

Ewelina MłynarskaDepartment of Nephrocardiology, Medical University of Lodz, 90-419 Łódź, Poland.ORCID 0000-0002-6799-4746
Kinga BojdoDepartment of Nephrocardiology, Medical University of Lodz, 90-419 Łódź, Poland.ORCID 0009-0002-1234-3409
Hanna FrankensteinDepartment of Nephrocardiology, Medical University of Lodz, 90-419 Łódź, Poland.
Katarzyna KrawirandaDepartment of Nephrocardiology, Medical University of Lodz, 90-419 Łódź, Poland.
Natalia KustosikDepartment of Nephrocardiology, Medical University of Lodz, 90-419 Łódź, Poland.ORCID 0009-0006-6075-9627
Wiktoria LisińskaDepartment of Nephrocardiology, Medical University of Lodz, 90-419 Łódź, Poland.
Jacek RyszDepartment of Nephrology, Hypertension and Internal Medicine, Medical University of Lodz, 90-549 Łodz, Poland.
Beata FranczykDepartment of Nephrocardiology, Medical University of Lodz, 90-419 Łódź, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial dysfunction plays a central role in the pathogenesis of cardiovascular diseases, driven by a complex interplay of oxidative stress, metabolic imbalances, and adipokine dysregulation. Excessive reactive oxygen species reduce nitric oxide bioavailability by impairing endothelial nitric oxide synthase function, leading to vascular inflammation and impaired vasodilation. Adipose tissue-derived hormones such as leptin, adiponectin, and resistin exert opposing effects on vascular homeostasis, influencing inflammation and oxidative stress in obesity and metabolic syndrome. Dyslipidemia, particularly through oxidized LDL, initiates endothelial injury and foam cell formation, accelerating atherosclerosis. Furthermore, hypertension and obesity exacerbate vascular dysfunction by disrupting the balance between vasodilators and vasoconstrictors, enhancing oxidative stress, and altering perivascular adipose tissue function. These interrelated mechanisms contribute to the progression of atherosclerotic cardiovascular disease and diabetic vascular complications. A deeper understanding of these processes is essential for developing targeted interventions to restore endothelial health and reduce cardiometabolic risk.

Indexed as

AtherosclerosisEndothelium, VascularHypertensionObesityAdipokinesAnimalsHumansOxidative StressReactive Oxygen SpeciesAdipokinesReactive Oxygen Speciesadipocytokinesatherosclerosisbiomarkerscardiometabolic diseasechemokinesdiabetesendothelial activationendothelial dysfunctionendothelial nitric oxide synthasevascular inflammation

Identifiers

PMID41155389
PMCPMC12564390

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.