Evidence mapPaperPMID 38488029Full record

ReviewMolecular medicine reports2024

Role and molecular mechanisms of SGLT2 inhibitors in pathological cardiac remodeling (Review).

Bixian Chen, Jing Guo, Hongmei Ye, Xinyu Wang, Yufei Feng

Open access · hybridAbstract readReview
In one paragraph

Review in Molecular medicine reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
11.4field-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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Novel Drug Targets in Diastolic Heart Disease.International journal of molecular sciences · 2025
    Review
  15. Article
  16. Observational
  17. Anti-Inflammatory Effects of SGLT2 Inhibitors: Focus on Macrophages.International journal of molecular sciences · 2025
    Review
  18. Article
  19. Article
  20. Article
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

5 authors at 2 institutions in 1 country.

Bixian Chen *Department of Pharmacy, Peking University People's Hospital, Beijing 100044, P.R. China.
Jing Guo *Department of Pharmacy, Peking University People's Hospital, Beijing 100044, P.R. China.
Hongmei YeDepartment of Pharmacy, Peking University People's Hospital, Beijing 100044, P.R. China.
Xinyu WangDepartment of Pharmacy, Peking University People's Hospital, Beijing 100044, P.R. China.
Yufei FengClinical Trial Institution, Peking University People's Hospital, Beijing 100044, P.R. China.
Peking University · CNPeking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular diseases are caused by pathological cardiac remodeling, which involves fibrosis, inflammation and cell dysfunction. This includes autophagy, apoptosis, oxidative stress, mitochondrial dysfunction, changes in energy metabolism, angiogenesis and dysregulation of signaling pathways. These changes in heart structure and/or function ultimately result in heart failure. In an effort to prevent this, multiple cardiovascular outcome trials have demonstrated the cardiac benefits of sodium‑glucose cotransporter type 2 inhibitors (SGLT2is), hypoglycemic drugs initially designed to treat type 2 diabetes mellitus. SGLT2is include empagliflozin and dapagliflozin, which are listed as guideline drugs in the 2021 European Guidelines for Heart Failure and the 2022 American Heart Association/American College of Cardiology/Heart Failure Society of America Guidelines for Heart Failure Management. In recent years, multiple studies using animal models have explored the mechanisms by which SGLT2is prevent cardiac remodeling. This article reviews the role of SGLT2is in cardiac remodeling induced by different etiologies to provide a guideline for further evaluation of the mechanisms underlying the inhibition of pathological cardiac remodeling by SGLT2is, as well as the development of novel drug targets.

Indexed as

Diabetes Mellitus, Type 2Heart FailureSodium-Glucose Transporter 2 InhibitorsAnimalsHumansHypoglycemic AgentsVentricular RemodelingHypoglycemic AgentsSodium-Glucose Transporter 2 Inhibitorscardiac fibroblastscardiac remodelingmolecular mechanismsmyocardial hypertrophySGLT2 inhibitors

Identifiers

PMID38488029
PMCPMC10955520
OpenAlexW4392651634

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.