Evidence map›Paper›PMID 38181714›Full record

ArticleBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2024

Cardioprotection by the adiponectin receptor agonist ALY688 in a preclinical mouse model of heart failure with reduced ejection fraction (HFrEF).

Sungji Cho, Keith Dadson, Hye Kyoung Sung, Oyeronke Ayansola, Ali Mirzaesmaeili, Nina Noskovicova, Yimu Zhao, Krisco Cheung, Milica Radisic, Boris Hinz and 4 more

Open access · goldAbstract read
In one paragraph

Article in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

12 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Cardioprotective Effects of Adiponectin-Stimulated Autophagy.Journal of lipid and atherosclerosis · 2025
    Review
  11. Article
  12. 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 at 5 institutions in 2 countries.

Sungji ChoDepartment of Biology, York University, Toronto, ON, Canada.
Keith DadsonDepartment of Biology, York University, Toronto, ON, Canada.
Hye Kyoung SungDepartment of Biology, York University, Toronto, ON, Canada.
Oyeronke AyansolaDepartment of Biology, York University, Toronto, ON, Canada.
Ali MirzaesmaeiliSchool of Kinesiology and Health Science, York University, Toronto, ON, Canada.
Nina NoskovicovaFaculty of Dentistry, University of Toronto, Toronto, ON M5S3E2, Canada.
Yimu ZhaoToronto General Hospital Research Institute, Toronto, ON M5G 2C4, Canada; Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, ON M5S 3G9, Canada.
Krisco CheungDepartment of Chemical Engineering and Applied Chemistry; University of Toronto, Toronto, ON M5S 3E5, Canada.
Milica RadisicToronto General Hospital Research Institute, Toronto, ON M5G 2C4, Canada; Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, ON M5S 3G9, Canada; Department of Chemical Engineering and Applied Chemistry; University of Toronto, Toronto, ON M5S 3E5, Canada.
Boris HinzFaculty of Dentistry, University of Toronto, Toronto, ON M5S3E2, Canada; Laboratory of Tissue Repair and Regeneration, Keenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, ON M5B 1T8, Canada.
Ali A Abdul SaterSchool of Kinesiology and Health Science, York University, Toronto, ON, Canada.
Henry H HsuAllysta Pharmaceuticals Inc. Bellevue, WA, USA.
Gary D LopaschukDepartment of Pediatrics, University of Alberta, Edmonton, AB, Canada.
Gary SweeneyDepartment of Biology, York University, Toronto, ON, Canada. Electronic address: gsweeney@yorku.ca.
York University · CAUniversity of Toronto · CABellevue Hospital Center · USSt. Michael's Hospital · CAUniversity of Alberta · CA

Funding

Engineering Vascularized Cardiac MuscleR01HL076485 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Gordana Vunjak-Novakovic · 2005 to 2026
$9.2M
NHLBI NIH HHS R01 HL076485
6 · The paper itself

Abstract

aimsAdiponectin has been shown to mediate cardioprotective effects and levels are typically reduced in patients with cardiometabolic disease. Hence, there has been intense interest in developing adiponectin-based therapeutics. The aim of this translational research study was to examine the functional significance of targeting adiponectin signaling with the adiponectin receptor agonist ALY688 in a mouse model of heart failure with reduced ejection fraction (HFrEF), and the mechanisms of cardiac remodeling leading to cardioprotection. METHODS AND

resultsWild-type mice were subjected to transverse aortic constriction (TAC) to induce left ventricular pressure overload (PO), or sham surgery, with or without daily subcutaneous ALY688-SR administration. Temporal analysis of cardiac function was conducted via weekly echocardiography for 5 weeks and we observed that ALY688 attenuated the PO-induced dysfunction. ALY688 also reduced cardiac hypertrophic remodeling, assessed via LV mass, heart weight to body weight ratio, cardiomyocyte cross sectional area, ANP and BNP levels. ALY688 also attenuated PO-induced changes in myosin light and heavy chain expression. Collagen content and myofibroblast profile indicated that fibrosis was attenuated by ALY688 with TIMP1 and scleraxis/periostin identified as potential mechanistic contributors. ALY688 reduced PO-induced elevation in circulating cytokines including IL-5, IL-13 and IL-17, and the chemoattractants MCP-1, MIP-1β, MIP-1alpha and MIP-3α. Assessment of myocardial transcript levels indicated that ALY688 suppressed PO-induced elevations in IL-6, TLR-4 and IL-1β, collectively indicating anti-inflammatory effects. Targeted metabolomic profiling indicated that ALY688 increased fatty acid mobilization and oxidation, increased betaine and putrescine plus decreased sphingomyelin and lysophospholipids, a profile indicative of improved insulin sensitivity.

conclusionThese results indicate that the adiponectin mimetic peptide ALY688 reduced PO-induced fibrosis, hypertrophy, inflammation and metabolic dysfunction and represents a promising therapeutic approach for treating HFrEF in a clinical setting.

Indexed as

Heart FailureAdiponectinAnimalsFibrosisHumansMiceMice, Inbred C57BLMyocytes, CardiacReceptors, AdiponectinStroke VolumeVentricular RemodelingAdiponectinReceptors, AdiponectinAdiponectinFibrosisHeart failureInflammationMetabolismTherapeutic

Identifiers

PMID38181714
PMCPMC12389264
OpenAlexW4390597508

What Socratic 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 Socratic graph.