Evidence map›Paper›PMID 33878400›Full record

ReviewMolecular metabolism2021

Insulin's actions on vascular tissues: Physiological effects and pathophysiological contributions to vascular complications of diabetes.

Jialin Fu, Marc Gregory Yu, Qian Li, Kyoungmin Park, George L King

Open access · goldAbstract readReview
In one paragraph

Review in Molecular metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

56 citing papers in PubMed, 89 citations in OpenAlex.

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  13. Co-segregation ofFrontiers in pediatrics · 2026
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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 1 institution in 1 country.

Jialin FuDianne Nunnally Hoppes Laboratory for Diabetes Complications, Section of Vascular Cell Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA, 02215, USA.
Marc Gregory YuDianne Nunnally Hoppes Laboratory for Diabetes Complications, Section of Vascular Cell Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA, 02215, USA.
Qian LiDianne Nunnally Hoppes Laboratory for Diabetes Complications, Section of Vascular Cell Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA, 02215, USA.
Kyoungmin ParkDianne Nunnally Hoppes Laboratory for Diabetes Complications, Section of Vascular Cell Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA, 02215, USA.
George L KingDianne Nunnally Hoppes Laboratory for Diabetes Complications, Section of Vascular Cell Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA, 02215, USA. Electronic address: George.King@joslin.harvard.edu.
Joslin Diabetes Center · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI JEAN E. SCHAFFER · 1986 to 2026
$50.5M
SELECTIVE INSULIN RESISTANCE--DIABETIC VASCULAR DISEASER01DK053105 · NIDDK · JOSLIN DIABETES CENTER · PI KING, GEORGE L · 1997 to 2017
$5.0M
Validation of Potential Protective Factors from Diabetic ComplicationsDP3DK094333 · NIDDK · JOSLIN DIABETES CENTER · PI KING, GEORGE L · 2011 to 2015
$4.1M
NIDDK NIH HHS DP3 DK094333NIDDK NIH HHS P30 DK036836NIDDK NIH HHS R01 DK053105
6 · The paper itself

Abstract

backgroundInsulin has been demonstrated to exert direct and indirect effects on vascular tissues. Its actions in vascular cells are mediated by two major pathways: the insulin receptor substrate 1/2-phosphoinositide-3 kinase/Akt (IRS1/2/PI3K/Akt) pathway and the Src/mitogen-activated protein kinase (MAPK) pathway, both of which contribute to the expression and distribution of metabolites, hormones, and cytokines. SCOPE OF REVIEW: In this review, we summarize the current understanding of insulin's physiological and pathophysiological actions and associated signaling pathways in vascular cells, mainly in endothelial cells (EC) and vascular smooth muscle cells (VSMC), and how these processes lead to selective insulin resistance. We also describe insulin's potential new signaling and biological effects derived from animal studies and cultured capillary and arterial EC, VSMC, and pericytes. We will not provide a detailed discussion of insulin's effects on the myocardium, insulin's structure, or its signaling pathways' various steps, since other articles in this issue discuss these areas in depth. MAJOR

conclusionsInsulin mediates many important functions on vascular cells via its receptors and signaling cascades. Its direct actions on EC and VSMC are important for transporting and communicating nutrients, cytokines, hormones, and other signaling molecules. These vascular actions are also important for regulating systemic fuel metabolism and energetics. Inhibiting or enhancing these pathways leads to selective insulin resistance, exacerbating the development of endothelial dysfunction, atherosclerosis, restenosis, poor wound healing, and even myocardial dysfunction. Targeted therapies to improve selective insulin resistance in EC and VSMC are thus needed to specifically mitigate these pathological processes.

Indexed as

Insulin ResistanceAnimalsDiabetic AngiopathiesDisease Models, AnimalEndothelial CellsEndothelium, VascularHumansInsulinInsulin Receptor Substrate ProteinsMAP Kinase Signaling SystemMuscle, Smooth, VascularMyocytes, Smooth MusclePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAKT1 protein, humanInsulinInsulin Receptor Substrate ProteinsIRS1 protein, humanIRS2 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCardiovascular complicationsCVDDiabetesInsulin resistance

Identifiers

PMID33878400
PMCPMC8513152
OpenAlexW3154496487

What OpenQuestion 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 OpenQuestion graph.