Evidence map›Paper›PMID 33378699›Full record

ReviewBiochimica et biophysica acta. Molecular basis of disease2021

Diabetic fibrosis.

Izabela Tuleta, Nikolaos G Frangogiannis

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Molecular basis of disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07734870 (Tirzepatide for Treatment of CCCA), which is not on this map. Cited by 130 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 2 pooled it
10.7field-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.

NCT07734870 phase2not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Tirzepatide for Treatment of CCCA

TypeinterventionalSponsorJohns Hopkins UniversityRan2026 to 2028Enrolled20ConditionsCentral Centrifugal Cicatricial Alopecia (CCCA)ArmsTirzepatide
3 · Its place in the literature

Who cites it

130 citing papers in PubMed, 2 syntheses or guidelines pooled it, 187 citations in OpenAlex.

  1. Pooled it
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  4. Article
  5. Binaphthoquinone attenuates myofibroblast transition of human ventricular cardiac fibroblastsThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
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70 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

Stable Isotope and Metabolomics CoreP60DK020541 · NIDDK · YESHIVA UNIVERSITY · PI PESSIN, JEFFREY E. · 1986 to 2014
$29.8M
Translational Research CoreP30DK020541 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STREAMSON C CHUA · 2015 to 2026
$27.7M
Chemokines in Healing Myocardial InfarctsR01HL076246 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI Nikolaos G Frangogiannis · 2005 to 2026
$9.5M
Resolution of Inflammation in healing Myocardial InfarctsR01HL085440 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI FRANGOGIANNIS, NIKOLAOS G · 2008 to 2025
$8.5M
Regulation of the TGF-beta superfamily in the remodeling and failing heartR01HL149407 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI FRANGOGIANNIS, NIKOLAOS G · 2020 to 2023
$2.2M
NHLBI NIH HHS R01 HL076246NHLBI NIH HHS R01 HL085440NHLBI NIH HHS R01 HL149407NIDDK NIH HHS P30 DK020541NIDDK NIH HHS P60 DK020541
6 · The paper itself

Abstract

Diabetes-associated morbidity and mortality is predominantly due to complications of the disease that may cause debilitating conditions, such as heart and renal failure, hepatic insufficiency, retinopathy or peripheral neuropathy. Fibrosis, the excessive and inappropriate deposition of extracellular matrix in various tissues, is commonly found in patients with advanced type 1 or type 2 diabetes, and may contribute to organ dysfunction. Hyperglycemia, lipotoxic injury and insulin resistance activate a fibrotic response, not only through direct stimulation of matrix synthesis by fibroblasts, but also by promoting a fibrogenic phenotype in immune and vascular cells, and possibly also by triggering epithelial and endothelial cell conversion to a fibroblast-like phenotype. High glucose stimulates several fibrogenic pathways, triggering reactive oxygen species generation, stimulating neurohumoral responses, activating growth factor cascades (such as TGF-β/Smad3 and PDGFs), inducing pro-inflammatory cytokines and chemokines, generating advanced glycation end-products (AGEs) and stimulating the AGE-RAGE axis, and upregulating fibrogenic matricellular proteins. Although diabetes-activated fibrogenic signaling has common characteristics in various tissues, some organs, such as the heart, kidney and liver develop more pronounced and clinically significant fibrosis. This review manuscript summarizes current knowledge on the cellular and molecular pathways involved in diabetic fibrosis, discussing the fundamental links between metabolic perturbations and fibrogenic activation, the basis for organ-specific differences, and the promises and challenges of anti-fibrotic therapies for diabetic patients.

Indexed as

AnimalsDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Disease ProgressionEpigenesis, GeneticFibroblastsFibrosisGlucoseHumansInflammationSignal TransductionGlucoseDiabetesExtracellular matrixFibroblastFibrosisGrowth factorsMatricellular proteins

Identifiers

PMID33378699
PMCPMC7867637
OpenAlexW4211053686

What OpenQuestion holds

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LicenceTDM
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.