Evidence map›Paper›PMID 30349977›Full record

ReviewHeart failure reviews2019

Diabetic cardiomyopathy: molecular mechanisms, detrimental effects of conventional treatment, and beneficial effects of natural therapy.

Brahmanaidu Parim, V V Sathibabu Uddandrao, Ganapathy Saravanan

Abstract readComparative StudyReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 1 pooled it
10.1field-weighted citation impact, top 1% 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

94 citing papers in PubMed, 1 synthesis or guideline pooled it, 205 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. snRNA-seq identifies Fmo2npj metabolic health and disease · 2026
    Article
  5. Review
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  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. α-ALA Attenuates Cardiac Injury in Diabetic Heart Disease Mice by Modulating Inflammation and AMPKα1.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Article
  18. Review
  19. Article
  20. Article

34 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

3 authors at 2 institutions in 1 country.

Brahmanaidu ParimAnimal Physiology and Biochemistry Laboratory, ICMR-National Animal Resource Facility for Biomedical Research (NARFBR), Hyderabad, Telangana, 500007, India. brahmanaiduparim@gmail.com.
V V Sathibabu UddandraoCenter for Biological Sciences, Department of Biochemistry, K.S. Rangasamy College of Arts and Science (Autonomous), Tiruchengode, Tamil Nadu, 637215, India.
Ganapathy SaravananCenter for Biological Sciences, Department of Biochemistry, K.S. Rangasamy College of Arts and Science (Autonomous), Tiruchengode, Tamil Nadu, 637215, India.
KS Rangasamy College of Arts and ScienceNational Institute of Animal Biotechnology · IN

Funding

Innovation in Science Pursuit for Inspired Research (INSPIRE), Department of Science and Technology (DST), Government of India DST/INSPIRE/04/2016/000893
6 · The paper itself

Abstract

abstarctDiabetic complications are among the largely exigent health problems currently. Cardiovascular complications, including diabetic cardiomyopathy (DCM), account for more than 80% of diabetic deaths. Investigators are exploring new therapeutic targets to slow or abate diabetes because of the growing occurrence and augmented risk of deaths due to its complications. Research on rodent models of type 1 and type 2 diabetes mellitus, and the use of genetic engineering techniques in mice and rats have significantly sophisticated for our understanding of the molecular mechanisms in human DCM. DCM is featured by pathophysiological mechanisms that are hyperglycemia, insulin resistance, oxidative stress, left ventricular hypertrophy, damaged left ventricular systolic and diastolic functions, myocardial fibrosis, endothelial dysfunction, myocyte cell death, autophagy, and endoplasmic reticulum stress. A number of molecular and cellular pathways, such as cardiac ubiquitin proteasome system, FoxO transcription factors, hexosamine biosynthetic pathway, polyol pathway, protein kinase C signaling, NF-κB signaling, peroxisome proliferator-activated receptor signaling, Nrf2 pathway, mitogen-activated protein kinase pathway, and micro RNAs, play a major role in DCM. Currently, there are a few drugs for the management of DCM and some of them have considerable adverse effects. So, researchers are focusing on the natural products to ameliorate it. Hence, in this review, we discuss the pathogical, molecular, and cellular mechanisms of DCM; the current diagnostic methods and treatments; adverse effects of conventional treatment; and beneficial effects of natural product-based therapeutics, which may pave the way to new treatment strategies. Graphical Abstract.

Indexed as

AnimalsAntibiotics, AntineoplasticAutopsyCardiomegalyDiabetes Mellitus, Type 2Diabetic CardiomyopathiesFibrosisGenetic EngineeringHumansHypertrophy, Left VentricularInjections, IntraperitonealMiceMice, Inbred C57BLModels, AnimalMyocardiumRatsAntibiotics, AntineoplasticStreptozocinCardiovascular disordersDiabetic cardiomyopathyDiabetic complicationsMedicinal plantsNatural products

Identifiers

PMID30349977
OpenAlexW2895826799

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.