Evidence map›Paper›PMID 28434143›Full record

ReviewCurrent diabetes reports2017

The mTOR Signaling Pathway in Myocardial Dysfunction in Type 2 Diabetes Mellitus.

Tomohiro Suhara, Yuichi Baba, Briana K Shimada, Jason K Higa, Takashi Matsui

Open access · greenAbstract readReview
In one paragraph

Review in Current diabetes reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. Physical Activity and Its Impact on Cardiometabolic Disorders.Handbook of experimental pharmacology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. A protein encoded by circular ZNF609 RNA induces acute kidney injury by activating the AKT/mTOR-autophagy pathway.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  13. mTOR Signaling Pathway in Bone Diseases Associated with Hyperglycemia.International journal of molecular sciences · 2023
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Montelukast and Acute Coronary Syndrome: The Endowed Drug.Pharmaceuticals (Basel, Switzerland) · 2022
    Review
  19. Activation of Rictor/mTORC2 signaling acts as a pivotal strategy to protect against sensorineural hearing loss.Proceedings of the National Academy of Sciences of the United States of America · 2022
    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 2 countries.

Tomohiro SuharaDepartment of Anatomy, Biochemistry & Physiology, John A. Burns School of Medicine, University of Hawaii at Manoa, 651 Ilalo St., BSB no. 110, Honolulu, HI, 96813, USA.
Yuichi BabaDepartment of Anatomy, Biochemistry & Physiology, John A. Burns School of Medicine, University of Hawaii at Manoa, 651 Ilalo St., BSB no. 110, Honolulu, HI, 96813, USA.
Briana K ShimadaDepartment of Anatomy, Biochemistry & Physiology, John A. Burns School of Medicine, University of Hawaii at Manoa, 651 Ilalo St., BSB no. 110, Honolulu, HI, 96813, USA.
Jason K HigaDepartment of Anatomy, Biochemistry & Physiology, John A. Burns School of Medicine, University of Hawaii at Manoa, 651 Ilalo St., BSB no. 110, Honolulu, HI, 96813, USA.
Takashi MatsuiDepartment of Anatomy, Biochemistry & Physiology, John A. Burns School of Medicine, University of Hawaii at Manoa, 651 Ilalo St., BSB no. 110, Honolulu, HI, 96813, USA. tmatsui@hawaii.edu.
University of Hawaiʻi at Mānoa · USKeio University · JP

Funding

Training in Cardiovascular Research at the University of HawaiiT32HL115505 · NHLBI · UNIVERSITY OF HAWAII AT MANOA · PI Michelle D Tallquist · 2012 to 2026
$3.8M
NHLBI NIH HHS T32 HL115505
6 · The paper itself

Abstract

purpose of reviewT2DM (type 2 diabetes mellitus) is a risk factor for heart failure. The mTOR (mechanistic target of rapamycin) is a key mediator of the insulin signaling pathway. We will discuss the role of mTOR in myocardial dysfunction in T2DM. RECENT

findingsIn T2DM, chronically activated mTOR induces multiple pathological events, including a negative feedback loop that suppresses IRS (insulin receptor substrate)-1. While short-term treatment with rapamycin, an mTOR inhibitor, is a promising strategy for cardiac diseases such as acute myocardial infarction and cardiac hypertrophy in T2DM, there are many concerns about chronic usage of rapamycin. Two mTOR complexes, mTORC1 and mTORC2, affect many molecules and processes via distinct signaling pathways that regulate cardiomyocyte function and survival. Understanding mechanisms underlying mTOR-mediated pathophysiological features in the heart is essential for developing effective therapies for cardiac diseases in the context of T2DM.

Indexed as

Diabetes Mellitus, Type 2Heart DiseasesHumansMyocardiumSignal TransductionTOR Serine-Threonine KinasesMTOR protein, humanTOR Serine-Threonine KinasesCardiovascular diseaseCell signalingDiabetes mellitusHeart failuremTORRapamycin

Identifiers

PMID28434143
PMCPMC8219468
OpenAlexW2605404328

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.