Evidence map›Paper›PMID 38898303›Full record

ArticleDiabetologia2024

eNAMPT is a novel therapeutic target for mitigation of coronary microvascular disease in type 2 diabetes.

Lei Gao, Francisco J Ramirez, Jody Tori O Cabrera, Mathews V Varghese, Makiko Watanabe, Atsumi Tsuji-Hosokawa, Qiuyu Zheng, Mingya Yang, Md Rahatullah Razan, Carrie L Kempf and 4 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Diabetologia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
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

14 authors.

Lei Gao *Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
Francisco J Ramirez *Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
Jody Tori O Cabrera *Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
Mathews V VargheseDepartment of Physiology, The University of Arizona, Tucson, AZ, USA.
Makiko WatanabeDepartment of Physiology, The University of Arizona, Tucson, AZ, USA.
Atsumi Tsuji-HosokawaDepartment of Physiology, The University of Arizona, Tucson, AZ, USA.
Qiuyu ZhengDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA.
Mingya YangDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA.
Md Rahatullah RazanDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA.
Carrie L KempfCenter for Inflammation Science and Systems Medicine, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, University of Florida, Jupiter, FL, USA.
Sara M CampCenter for Inflammation Science and Systems Medicine, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, University of Florida, Jupiter, FL, USA.
Jian WangState Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Joe G N GarciaCenter for Inflammation Science and Systems Medicine, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, University of Florida, Jupiter, FL, USA.
Ayako MakinoDepartment of Medicine, University of California, San Diego, La Jolla, CA, USA. ay.makino@ufl.edu.ORCID http://orcid.org/0000-0003-1259-8604

Funding

Structure-Function Analysis of nmMLCK in EC Barrier ResponsesP01HL126609 · NHLBI · UNIVERSITY OF FLORIDA · PI Joe G. N. Garcia · 2016 to 2026
$24.4M
Novel Involvement of NAMPT and TLR4 in PAH Vascular RemodelingR01HL141387 · NHLBI · UNIVERSITY OF FLORIDA · PI Joe G. N. Garcia, Ayako Makino · 2019 to 2026
$3.8M
Coronary Endothelial Cell Dysfunction in Diabetes: Role of MFGE8R01HL142214 · NHLBI · UNIVERSITY OF FLORIDA · PI Yun Sok Lee, Ayako Makino · 2018 to 2026
$3.2M
Role of Gap Junction in Hypoxia-induced Pulmonary HypertensionR01HL146764 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MAKINO, AYAKO · 2019 to 2022
$1.6M
Congressionally Directed Medical Research Programs W81XWH2110472NHLBI NIH HHS HL126609NHLBI NIH HHS HL141387NHLBI NIH HHS HL142214NHLBI NIH HHS HL146764NHLBI NIH HHS P01 HL126609NHLBI NIH HHS R01 HL141387NHLBI NIH HHS R01 HL142214NHLBI NIH HHS R01 HL146764
6 · The paper itself

Abstract

aims/hypothesisIndividuals with diabetes are at high risk of cardiovascular complications, which significantly increase morbidity/mortality. Coronary microvascular disease (CMD) is recognised as a critical contributor to the increased cardiac mortality observed in people with diabetes. Therefore, there is an urgent need for treatments that are specific to CMD. eNAMPT (extracellular nicotinamide phosphoribosyltransferase) is a damage-associated molecular pattern and TLR4 ligand, whose plasma levels are elevated in people with diabetes. This study was thus designed to investigate the pathogenic role of intracellular nicotinamide phosphoribosyltransferase (iNAMPT) and eNAMPT in promoting the development of CMD in a preclinical murine model of type 2 diabetes.

methodsAn inducible type 2 diabetic mouse model was generated by a single injection of low-dose streptozocin (75 mg/kg, i.p.) combined with a high-fat diet for 16 weeks. The in vivo effects of i/eNAMPT inhibition on cardiac endothelial cell (CEC) function were evaluated by using Nampt

resultsAs expected, diabetic wild-type mice exhibited significantly lower coronary flow velocity reserve (CFVR), a determinant of coronary microvascular function, compared with control wild-type mice. eNAMPT plasma levels or expression in CECs were significantly greater in diabetic mice than in control mice. Furthermore, in comparison with diabetic wild-type mice, diabetic Nampt CONCLUSIONS/

interpretationThese data indicate that increased i/eNAMPT expression contributes to the development of diabetic coronary microvascular dysfunction, and provide compelling support for eNAMPT inhibition as a novel and effective therapeutic strategy for CMD in diabetes.

Indexed as

Diabetes Mellitus, Type 2Nicotinamide PhosphoribosyltransferaseAnimalsCoronary VesselsCytokinesDiabetes Mellitus, ExperimentalEndothelial CellsMaleMiceMice, Inbred C57BLCytokinesNicotinamide Phosphoribosyltransferasenicotinamide phosphoribosyltransferase, mouseCoronary blood flowEndothelial cell functionMicrovascular complicationsPBEFType 2 diabetesVisfatin

Identifiers

PMID38898303
PMCPMC11410976

What Socratic holds

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Registered trials

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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.