Evidence map›Paper›PMID 25994075›Full record

ArticleDiabetologia2015

Silencing of miR-195 reduces diabetic cardiomyopathy in C57BL/6 mice.

Dong Zheng, Jian Ma, Yong Yu, Minghui Li, Rui Ni, Grace Wang, Ruizhen Chen, Jianmin Li, Guo-Chang Fan, James C Lacefield and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

97 citing papers in PubMed, 1 synthesis or guideline pooled it, 153 citations in OpenAlex.

  1. Pooled it
  2. Molecular Mechanisms Governing Vascular Function in Heart Failure.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Roles of microRNAs in cardiorenal syndrome.Molecular and cellular biochemistry · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Mechanistic insight into the role of cardiac-enriched microRNAs in diabetic heart injury.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Molecular Basis of Cardiomyopathies in Type 2 Diabetes.International journal of molecular sciences · 2024
    Review
  18. Roles of non-coding RNA in diabetic cardiomyopathy.Cardiovascular diabetology · 2024
    Review
  19. Article
  20. Article

37 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

11 authors at 7 institutions in 3 countries.

Dong ZhengInstitutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu Province, China, 215123.
Jian Ma
Yong Yu
Minghui Li
Rui Ni
Grace Wang
Ruizhen Chen
Jianmin Li
Guo-Chang Fan
James C Lacefield
Tianqing Peng
Lawson Health Research Institute · CASoochow University · CNSun Yat-sen University · CNWestern University · CAThe First Affiliated Hospital, Sun Yat-sen University · CNUniversity of Cincinnati Medical Center · USWenzhou Medical University · CN

Funding

Roles of Hsp20-Exosomes in Myocardial AngiogenesisR01HL087861 · NHLBI · UNIVERSITY OF CINCINNATI · PI FAN, GUO-CHANG · 2007 to 2017
$4.2M
Duplex miR-223 and Exosomes in SepsisR01GM112930 · NIGMS · UNIVERSITY OF CINCINNATI · PI FAN, GUO-CHANG · 2015 to 2018
$1.2M
Canadian Institutes of Health Research MOP-133657NHLBI NIH HHS HL-087861NHLBI NIH HHS R01 HL087861NIGMS NIH HHS R01 GM112930
6 · The paper itself

Abstract

aims/hypothesisMicroRNAs (miRs) have been suggested as potential therapeutic targets for heart diseases. Inhibition of miR-195 prevents apoptosis in cardiomyocytes stimulated with palmitate and transgenic overexpression of miR-195 induces cardiac hypertrophy and heart failure. We investigated whether silencing of miR-195 reduces diabetic cardiomyopathy in a mouse model of streptozotocin (STZ)-induced type 1 diabetes.

methodsType 1 diabetes was induced in C57BL/6 mice (male, 2 months old) by injections of STZ.

resultsMiR-195 expression was increased and levels of its target proteins (B cell leukaemia/lymphoma 2 and sirtuin 1) were decreased in STZ-induced type 1 and db/db type 2 diabetic mouse hearts. Systemically delivering an anti-miR-195 construct knocked down miR-195 expression in the heart, reduced caspase-3 activity, decreased oxidative stress, attenuated myocardial hypertrophy and improved myocardial function in STZ-induced mice with a concurrent upregulation of B cell leukaemia/lymphoma 2 and sirtuin 1. Diabetes reduced myocardial capillary density and decreased maximal coronary blood flow in mice. Knockdown of miR-195 increased myocardial capillary density and improved maximal coronary blood flow in diabetic mice. Upregulation of miR-195 sufficiently induced apoptosis in cardiomyocytes and attenuated the angiogenesis of cardiac endothelial cells in vitro. Furthermore, inhibition of miR-195 prevented apoptosis in cardiac endothelial cells in response to NEFA, an important feature of diabetes. CONCLUSIONS/

interpretationTherapeutic silencing of miR-195 reduces myocardial hypertrophy and improves coronary blood flow and myocardial function in diabetes, at least in part by reducing oxidative damage, inhibiting apoptosis and promoting angiogenesis. Thus, miR-195 may represent an alternative therapeutic target for diabetic heart diseases.

Indexed as

AnimalsCaspase 3Diabetes Mellitus, ExperimentalDiabetic CardiomyopathiesGene SilencingMaleMiceMice, Inbred C57BLMicroRNAsMyocardiumMyocytes, CardiacOxidative StressProto-Oncogene Proteins c-bcl-2Sirtuin 1Bcl2 protein, mouseCaspase 3MicroRNAsMIRN195a microRNA, mouseProto-Oncogene Proteins c-bcl-2Sirtuin 1

Identifiers

PMID25994075
PMCPMC4499474
OpenAlexW330316361

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.