Evidence map›Paper›PMID 35476352›Full record

ReviewReproductive sciences (Thousand Oaks, Calif.)2022

Inflammatory MicroRNAs and the Pathophysiology of Endometriosis and Atherosclerosis: Common Pathways and Future Directions Towards Elucidating the Relationship.

Zubeen D Azari, Fatimah Aljubran, Warren B Nothnick

Abstract readReview
PubMed Publisher
In one paragraph

Review in Reproductive sciences (Thousand Oaks, Calif.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Early atherogenesis: In search of etiology.International journal of cardiology. Cardiovascular risk and prevention · 2026
    Review
  2. Endometriosis: An Immunologist's Perspective.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Downregulation ofInternational journal of molecular sciences · 2023
    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

3 authors at 2 institutions in 1 country.

Zubeen D Azari *Kansas City University of Medicine and Biosciences, Kansas City, MO, 64106, USA.
Fatimah Aljubran *Department of Molecular and Integrative Physiology, Institute for Reproductive and Perinatal Sciences, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
Warren B NothnickDepartment of Molecular and Integrative Physiology, Institute for Reproductive and Perinatal Sciences, University of Kansas Medical Center, Kansas City, KS, 66160, USA. wnothnic@kumc.edu.
University of Kansas Medical Center · USKansas City University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging data indicates an association between endometriosis and subclinical atherosclerosis, with women with endometriosis at a higher risk for cardiovascular disease later in life. Inflammation is proposed to play a central role in the pathophysiology of both diseases and elevated levels of systemic pro-inflammatory cytokines including macrophage migration inhibitory factor (MIF), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) are well documented. However, a thorough understanding on the mediators and mechanisms which contribute to altered cytokine expression in both diseases remain poorly understood. MicroRNAs (miRNAs) are important post-transcriptional regulators of inflammatory pathways and numerous studies have reported altered circulating levels of miRNAs in both endometriosis and atherosclerosis. Potential contribution of miRNA-mediated inflammatory cascades common to the pathophysiology of both diseases has not been evaluated but could offer insight into common pathways and early manifestation relevant to both diseases which may help understand cause and effect. In this review, we discuss and summarize differentially expressed inflammatory circulating miRNAs in endometriosis subjects, compare this profile to that of circulating levels associated with atherosclerosis when possible, and then discuss mechanistic studies focusing on these miRNAs in relevant cell, tissue, and animal models. We conclude by discussing the potential utility of targeting the relevant miRNAs in the MIF-IL-6-TNF-α pathway as therapeutic options and offer insight into future studies which will help us better understand not only the role of these miRNAs in the pathophysiology of both endometriosis and atherosclerosis but also commonality between both diseases.

Indexed as

AtherosclerosisEndometriosisMicroRNAsAnimalsFemaleHumansInterleukin-6Tumor Necrosis Factor-alphaInterleukin-6MicroRNAsTumor Necrosis Factor-alphaAtherosclerosisCytokineEndometriosisInflammationmiRNA

Identifiers

PMID35476352
OpenAlexW4225016296

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.