Evidence mapPaperPMID 34331987Full record

ReviewAdvanced drug delivery reviews2021

Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities.

Izabela Tuleta, Nikolaos G Frangogiannis

Open access · greenAbstract readReview
In one paragraph

Review in Advanced drug delivery reviews, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
14.1field-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

79 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Immunometabolic Remodeling in Ischemic and Non-Ischemic Heart Failure.Journal of cardiovascular translational research · 2026
    Review
  7. Electrostatic lipidopathy drives human diabetic heart failure.Cardiovascular diabetology. Endocrinology reports · 2026
    Article
  8. Review
  9. Mechanical interplay between adipose tissues and disease progression.Bioengineering & translational medicine · 2026
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

19 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

2 authors at 1 institution in 1 country.

Izabela TuletaThe Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, Bronx NY, USA.
Nikolaos G FrangogiannisThe Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, Bronx NY, USA. Electronic address: nikolaos.frangogiannis@einsteinmed.org.
Albert Einstein College of Medicine · US

Funding

PROMOTING OPHTHALMIC SCREENING IN MANAGED CAREP60DK020541 · YESHIVA UNIVERSITY · 1986 to 2005
$12.6M
NYR-Diabetes Research Center (NYR-DRC)P30DK020541 · ALBERT EINSTEIN COLLEGE OF MEDICINE · 2025 to 2025
$2.4M
Resolution of inflammation in healing myocardial infarctsR01HL085440 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · 2023 to 2025
$2.2M
Chemokines in Healing Myocardial InfarctsR01HL076246 · NHLBI · BAYLOR COLLEGE OF MEDICINE · 2005 to 2025
$2.2M
NHLBI NIH HHS R01 HL076246NHLBI NIH HHS R01 HL085440NHLBI NIH HHS R01 HL149407NIDDK NIH HHS P30 DK020541
6 · The paper itself

Abstract

In patients with diabetes, myocardial fibrosis may contribute to the pathogenesis of heart failure and arrhythmogenesis, increasing ventricular stiffness and delaying conduction. Diabetic myocardial fibrosis involves effects of hyperglycemia, lipotoxicity and insulin resistance on cardiac fibroblasts, directly resulting in increased matrix secretion, and activation of paracrine signaling in cardiomyocytes, immune and vascular cells, that release fibroblast-activating mediators. Neurohumoral pathways, cytokines, growth factors, oxidative stress, advanced glycation end-products (AGEs), and matricellular proteins have been implicated in diabetic fibrosis; however, the molecular links between the metabolic perturbations and activation of a fibrogenic program remain poorly understood. Although existing therapies using glucose- and lipid-lowering agents and neurohumoral inhibition may act in part by attenuating myocardial collagen deposition, specific therapies targeting the fibrotic response are lacking. This review manuscript discusses the clinical significance, molecular mechanisms and cell biology of diabetic cardiac fibrosis and proposes therapeutic targets that may attenuate the fibrotic response, preventing heart failure progression.

Indexed as

AnimalsDiabetic CardiomyopathiesFibrosisHumansMyocardiumDiabetesFibroblastFibrosisGlucose-lowering agentsHeart failureHyperglycemiaInflammationLipotoxicityOxidative stress

Identifiers

PMID34331987
PMCPMC8444077
OpenAlexW3183979618

What Socratic 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 Socratic graph.