Evidence map›Paper›PMID 25689084›Full record

ReviewJournal of cardiovascular medicine (Hagerstown, Md.)2015

The two faces of miR-29.

Anna Ślusarz, Lakshmi Pulakat

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cardiovascular medicine (Hagerstown, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
3.3field-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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. miRNA: A Promising Therapeutic Target in Cancer.International journal of molecular sciences · 2022
    Review
  15. Review
  16. Review
  17. Insulin Resistance and Cancer: In Search for a Causal Link.International journal of molecular sciences · 2021
    Review
  18. Role of the microRNA-29 family in myocardial fibrosis.Journal of physiology and biochemistry · 2021
    Review
  19. Article
  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

2 authors at 1 institution in 1 country.

Anna ŚlusarzaDepartment of Medicine bDepartment of Biochemistry, University of Missouri cHarry S. Truman Memorial Veterans Affairs Hospital dDepartment of Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri, USA.
Lakshmi Pulakat
Harry S. Truman Memorial Veterans' Hospital · US

Funding

The mTORCI-miR-29-AT2R axis in cardiovascular diseasesR01HL118376 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI PULAKAT, LAKSHMIDEVI · 2013 to 2017
$2.0M
NHLBI NIH HHS 1R01HL118376-01NHLBI NIH HHS R01 HL118376
6 · The paper itself

Abstract

Diabetes mellitus is a metabolic homeostasis disease that contributes to additional comorbidities such as cardiovascular disease (CVD) and cancer. It has a long undiagnosed latent period during which there can be irreparable damage to the pancreas and cardiovascular tissues. Recent studies have highlighted the roles of several microRNAs in CVD. Determining the microRNAs that link diabetes mellitus and CVD is an important topic to be explored. In the present review, we discuss the microRNAs that contribute to the progression of diabetes mellitus and CVD and focus on the miR-29 family microRNAs whose expression is upregulated by hyperglycemia and proinflammatory cytokines, the hallmarks of diabetes mellitus. Upregulation of miR-29 expression is a key factor in the loss of pancreatic β cells and development of the first stage of type 1 diabetes mellitus (T1DM). Additionally, miR-29-mediated suppression of myeloid cell leukemia 1 (MCL-1), an important prosurvival protein, underlies Marfan's syndrome, abdominal aortic aneurysm, and diabetes mellitus-associated cardiomyocyte disorganization. Suppression of miR-29 expression and subsequent increase in the prosurvival MCL-1, however, promotes tumor development. Therefore, miR-29 mimics that suppress MCL-1 are hailed as tumor suppressors. The critical question is whether an increase in miR-29 levels is well tolerated in conditions of comorbidities in which insulin resistance is an underlying disease. In light of increasing awareness of the interconnection of diabetes mellitus, CVD, and cancer, it is of utmost importance to understand the mechanism of action of current treatment options on all of the comorbidities and careful evaluation of cardiovascular toxicity must accompany any treatment paradigm that increases miR-29 levels.

Indexed as

AnimalsCardiovascular DiseasesDiabetes ComplicationsDiabetes MellitusDiabetic AngiopathiesGene Expression RegulationGenetic Predisposition to DiseaseHumansImmunosuppressive AgentsMicroRNAsMyeloid Cell Leukemia Sequence 1 ProteinNeoplasmsSirolimusImmunosuppressive AgentsMCL1 protein, humanMicroRNAsMIRN29a microRNA, humanMyeloid Cell Leukemia Sequence 1 ProteinSirolimus

Identifiers

PMID25689084
PMCPMC4449311
OpenAlexW2048071448

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.