Evidence map›Paper›PMID 28676675›Full record

ArticleScientific reports2017

HMGCS2 is a key ketogenic enzyme potentially involved in type 1 diabetes with high cardiovascular risk.

Sanket Kumar Shukla, Weijing Liu, Kunal Sikder, Sankar Addya, Amrita Sarkar, Yidong Wei, Khadija Rafiq

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  7. Maladaptive Peripheral Ketogenesis in Schwann Cells Mediated by CBAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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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

7 authors at 2 institutions in 2 countries.

Sanket Kumar ShuklaDepartment of Medicine, Center of Translational Medicine, Thomas Jefferson University, Philadelphia, PA-19107, USA.
Weijing LiuInternal Medicine-Cardiovascular Department, Shanghai Tenth People's Hospital, Middle of Yanchang Road, Zhabei district, Shanghai, China.
Kunal SikderDepartment of Medicine, Center of Translational Medicine, Thomas Jefferson University, Philadelphia, PA-19107, USA.
Sankar AddyaKimmel Cancer Centre, Thomas Jefferson University, Philadelphia, PA-19107, USA.
Amrita SarkarDepartment of Medicine, Center of Translational Medicine, Thomas Jefferson University, Philadelphia, PA-19107, USA.
Yidong WeiDepartment of Cardiology, Shanghai Tenth People's Hospital of Tongji University, 301 Yanchang Road, Shanghai, China.
Khadija RafiqDepartment of Medicine, Center of Translational Medicine, Thomas Jefferson University, Philadelphia, PA-19107, USA. Khadija.Rafiq@jefferson.edu.
Thomas Jefferson University · USShanghai Tenth People's Hospital · CN

Funding

Inflammatory Proteases and Diabetic CardiomyopathyR01HL111278 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI RAFIQ, KHADIJA · 2013 to 2017
$1.9M
NHLBI NIH HHS R01 HL111278
6 · The paper itself

Abstract

Diabetes increases the risk of Cardio-vascular disease (CVD). CVD is more prevalent in type 2 diabetes (T2D) than type 1 diabetes (T1D), but the mortality risk is higher in T1D than in T2D. The pathophysiology of CVD in T1D is poorly defined. To learn more about biological pathways that are potentially involved in T1D with cardiac dysfunction, we sought to identify differentially expressed genes in the T1D heart. Our study used T1D mice with severe hyperglycemia along with significant deficits in echocardiographic measurements. Microarray analysis of heart tissue RNA revealed that the T1D mice differentially expressed 10 genes compared to control. Using Ingenuity Pathway Analysis (IPA), we showed that these genes were significantly involved in ketogenesis, cardiovascular disease, apoptosis and other toxicology functions. Of these 10 genes, the 3-Hydroxy-3-Methylglutaryl-CoA Synthase 2 (HMGCS2) was the highest upregulated gene in T1D heart. IPA analysis showed that HMGCS2 was center to many biological networks and pathways. Our data also suggested that apart from heart, the expression of HMGCS2 was also different in kidney and spleen between control and STZ treated mice. In conclusion, The HMGCS2 molecule may potentially be involved in T1D induced cardiac dysfunction.

Indexed as

AnimalsCardiovascular DiseasesComputational BiologyDiabetes Mellitus, Type 1EchocardiographyGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksHemodynamicsHumansHydroxymethylglutaryl-CoA SynthaseKetone BodiesMaleMiceMolecular Sequence AnnotationTranscriptomeHMGCS2 protein, humanHydroxymethylglutaryl-CoA SynthaseKetone Bodies

Identifiers

PMID28676675
PMCPMC5496911
OpenAlexW2731541918

What Socratic holds

Textmetadata
LicenceCC BY
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.