Evidence map›Paper›PMID 23034391›Full record

ArticleAmerican journal of physiology. Cell physiology2012

miR-141 as a regulator of the mitochondrial phosphate carrier (Slc25a3) in the type 1 diabetic heart.

Walter A Baseler, Dharendra Thapa, Rajaganapathi Jagannathan, Erinne R Dabkowski, Tara L Croston, John M Hollander

2 registry-linked trialsAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 72 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 2 pooled it
4.9field-weighted citation impact, top 4% 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.

NCT02611258 phase2completednot on this mapstarted 2016, after this paper: background citation

Study on New Insights in Remodeling of Endocrine Cardiomyopathies: Intramyocardial, Molecular and Neuroendocrine Assessment in Response to Chronic Inhibition of Cyclic GMP Phosphodiesterase 5A in Cushing's Syndrome

TypeinterventionalSponsorAndrea M. IsidoriRan2016 to 2021Enrolled18ConditionsCushing's Syndrome CardiomyopathyArmsTadalafil
NCT02611336 phase2completednot on this mapstarted 2016, after this paper: background citation

Study on New Insights in Remodeling of Endocrine Cardiomyopathies: ASsessmentt of Intramyocardial, Molecular and NeUroendocrine Parameters in Response to Chronic Inhibition of Cyclic GMP Phosphodiesterase 5A in AcroMegaly

TypeinterventionalSponsorAndrea M. IsidoriRan2016 to 2021Enrolled15ConditionsAcromegaly CardiomyopathyArmsTadalafil
3 · Its place in the literature

Who cites it

72 citing papers in PubMed, 2 syntheses or guidelines pooled it, 124 citations in OpenAlex.

  1. Noncoding RNA as potential therapeutics to rescue mitochondrial dysfunction in cardiovascular diseases.American journal of physiology. Heart and circulatory physiology · 2025
    Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Mechanistic insight into the role of cardiac-enriched microRNAs in diabetic heart injury.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Cardiac Metabolism and MiRNA Interference.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Article
  18. Effects of altered cellular ultrastructure on energy metabolism in diabetic cardiomyopathy: anPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022
    Article
  19. Article
  20. Review

12 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

6 authors at 1 institution in 1 country.

Walter A BaselerCenter for Cardiovascular and Respiratory Sciences, Division of Exercise Physiology, West Virginia University School of Medicine, Morgantown, WV 26506, USA.
Dharendra Thapa
Rajaganapathi Jagannathan
Erinne R Dabkowski
Tara L Croston
John M Hollander
West Virginia University · US

Funding

Mechanisms of Diabetic Cardiomyopathy: Mitochondria Subpopulations Brought to FocDP2DK083095 · NIDDK · WEST VIRGINIA UNIVERSITY · PI HOLLANDER, JOHN M · 2008 to 2010
$2.3M
Research Training in Cardiovascular and Pulmonary DiseasesT32HL090610 · NHLBI · WEST VIRGINIA UNIVERSITY · PI MUSTAFA, S. JAMAL · 2008 to 2012
$1.5M
NHLBI NIH HHS T32 HL090610NHLBI NIH HHS T32HL090610NIDDK NIH HHS DP2-DK-083095
6 · The paper itself

Abstract

Dysfunctional mitochondria are central in the pathogenesis of diabetic cardiomyopathy. Mitochondrial proteomic alterations resulting from diabetes mellitus have been reported although the mechanisms driving changes in proteomic signatures are unknown. microRNAs (miRNAs) have been considered as potential regulators of proteins. The goal of this study was to determine whether miRNAs play a role in diabetes-induced mitochondrial proteomic alterations. Quanitative RT-PCR miRNA screening in diabetic mice, 5 wk following multiple low-dose streptozotocin treatment was associated with alteration in the expression of 29 miRNAs in the diabetic heart compared with control. Among those miRNAs upregulated in the diabetic heart was miR-141 (P < 0.002). miRNA target prediction analyses identified miR-141 as a potential regulator of the inner mitochondrial membrane phosphate transporter, solute carrier family 25 member 3 (Slc25a3), which provides inorganic phosphate to the mitochondrial matrix and is essential for ATP production. With the use of a luciferase reporter construct with a Slc25a3 3'-untranslated region (UTR) target sequence, overexpression of miR-141 downregulated luciferase activity levels confirming miR-141/Slc25a3 3'-UTR binding. miR-141 overexpression in HL-1 cells elicited a decrease in Slc25a3 protein content, ATP production and a decrease in ATP synthase activity, similar to the diabetic phenotype (P < 0.05, for both). Diabetic interfibrillar mitochondria (IFM) displayed decreased Slc25a3 protein content, which was inversely correlated with increased miR-141 expression. Further, diabetic IFM ATP synthase activity was also decreased (P < 0.05). Together these results indicate that miR-141 can regulate Slc25a3 protein expression in the diabetic heart. Further, diabetes-induced miRNA changes may influence mitochondrial proteomes and functional processes such as mitochondrial ATP production.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetic CardiomyopathiesMaleMiceMicroRNAsMitochondria, HeartMitochondrial ProteinsMitochondrial Proton-Translocating ATPasesPhosphate Transport ProteinsMicroRNAsMirn141 microRNA, mouseMitochondrial ProteinsMitochondrial Proton-Translocating ATPasesPhosphate Transport ProteinsSLC25A3 protein, human

Identifiers

PMID23034391
PMCPMC3532490
OpenAlexW2127032769

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.