Evidence map›Paper›PMID 32359903›Full record

ArticleThe Journal of thoracic and cardiovascular surgery2022

Calpain inhibition decreases myocardial fibrosis in chronically ischemic hypercholesterolemic swine.

Brittany A Potz, Ashraf A Sabe, Sharif A Sabe, Isabella J Lawandy, M Ruhul Abid, Richard T Clements, Frank W Sellke

Open access · greenAbstract read
In one paragraph

Article in The Journal of thoracic and cardiovascular surgery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. Observational
  4. Article
  5. Article
  6. Review
  7. Article
  8. Calpains as Potential Therapeutic Targets for Myocardial Hypertrophy.International journal of molecular sciences · 2022
    Review
  9. Heat Shock Protein 90 as Therapeutic Target for CVDs and Heart Ageing.International journal of molecular sciences · 2022
    Review
  10. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Brittany A PotzDivision of Cardiothoracic Surgery, Department of Surgery, Cardiovascular Research Center, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, RI.
Ashraf A SabeDivision of Cardiothoracic Surgery, Department of Surgery, Cardiovascular Research Center, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, RI.
Sharif A SabeDivision of Cardiothoracic Surgery, Department of Surgery, Cardiovascular Research Center, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, RI.
Isabella J LawandyDivision of Cardiothoracic Surgery, Department of Surgery, Cardiovascular Research Center, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, RI.
M Ruhul AbidDivision of Cardiothoracic Surgery, Department of Surgery, Cardiovascular Research Center, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, RI.
Richard T ClementsDivision of Cardiothoracic Surgery, Department of Surgery, Cardiovascular Research Center, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, RI.
Frank W SellkeDivision of Cardiothoracic Surgery, Department of Surgery, Cardiovascular Research Center, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, RI. Electronic address: fsellke@lifespan.org.
Rhode Island Hospital · USBrown University · US

Funding

Uncoupling of IL-1 beta and VEGF-A Crosstalk Contributes to Impaired Arteriogenesis Response to Ischemia in Chronic Diabetes MellitusP20GM103652 · NIGMS · OCEAN STATE RESEARCH INSTITUTE, INC. · PI CHOUDHARY, GAURAV, HARRINGTON, ELIZABETH O · 2013 to 2022
$21.3M
Effect of Cardioplegia and Cardiopulmonary Bypass on Coronary Microvascular ReactivityR01HL046716 · NHLBI · RHODE ISLAND HOSPITAL · PI SELLKE, FRANK W · 1997 to 2023
$8.5M
Vascular Dysfunction in Myocardial Ischemia and Metabolic SyndromeR01HL128831 · NHLBI · RHODE ISLAND HOSPITAL · PI SELLKE, FRANK W, USHEVA-SIMIDJIYSKA, ANNY · 2016 to 2025
$5.7M
Trauma and Inflammation Research TrainingT32GM065085 · NIGMS · RHODE ISLAND HOSPITAL · PI Alfred Ayala · 2004 to 2026
$3.2M
Brown CardioPulmonary Research Training ProgramT32HL094300 · NHLBI · RHODE ISLAND HOSPITAL · PI KOREN, GIDEON · 2008 to 2012
$2.2M
Surgical Cardioprotection Through BKCa-Dependent Modulation of Mitochondrial SupercomplexesR01HL135236 · NHLBI · UNIVERSITY OF RHODE ISLAND · PI CLEMENTS, RICHARD T · 2018 to 2021
$1.9M
Short-Term Training Program to Increase Diversity in Health-Related ResearchR25HL088992 · NHLBI · BROWN UNIVERSITY · PI ABID, RUHUL, DIAZ, JOSEPH A · 2007 to 2024
$1.9M
Sub-cellular Targeting of Endothelial ROS in Myocardial IschemiaR01HL133624 · NHLBI · RHODE ISLAND HOSPITAL · PI ABID, RUHUL · 2017 to 2020
$1.6M
NHLBI NIH HHS R01 HL046716NHLBI NIH HHS R01 HL128831NHLBI NIH HHS R01 HL133624NHLBI NIH HHS R01 HL135236NHLBI NIH HHS R25 HL088992NHLBI NIH HHS T32 HL094300NIGMS NIH HHS P20 GM103652NIGMS NIH HHS T32 GM065085
6 · The paper itself

Abstract

objectivesCalpain activation during ischemia is known to play critical roles in myocardial remodeling. We hypothesize that calpain inhibition (CI) may serve to reverse and/or prevent fibrosis in chronically ischemic myocardium.

methodsYorkshire swine were fed a high-cholesterol diet for 4 weeks followed by placement of an ameroid constrictor on the left circumflex artery to induce myocardial ischemia. 3 weeks later, animals received either: no drug; high-cholesterol control group (CON; n = 8); low-dose CI (0.12 mg/kg; LCI, n = 9); or high-dose CI (0.25 mg/kg; HCI, n = 8). The high-cholesterol diet and CI were continued for 5 weeks, after which myocardial tissue was harvested. Tissue samples were analyzed by western blot for changes in protein content.

resultsIn the setting of hypercholesterolemia and chronic myocardial ischemia, CI decreased the expression of collagen in ischemic and nonischemic myocardial tissue. This reduced collagen content was associated with a corresponding decrease in Jak/STAT/MCP-1 signaling pathway, suggesting a role for Jak 2 signaling in calpain activity. CI also decreases the expression of focal adhesion proteins (vinculin) and stabilizes the expression of cytoskeletal and structural proteins (N-cadherin, α-fodrin, desmin, vimentin, filamin, troponin-I). CI had no significant effect on metabolic and hemodynamic parameters.

conclusionsCalpain inhibition may be a beneficial medical therapy to decrease collagen formation in patients with coronary artery disease and associated comorbidities.

Indexed as

CollagenMyocardiumVentricular RemodelingAnimalsCalpainChemokine CCL2Coronary Artery DiseaseDisease Models, AnimalFibrosisGlycoproteinsHypercholesterolemiaJanus Kinase 2Myocardial IschemiaSignal TransductionSTAT Transcription FactorsSwineCalpaincalpain inhibitorsChemokine CCL2CollagenGlycoproteinsJanus Kinase 2STAT Transcription Factorschronic myocardial ischemiacollagenfibrosis calpain inhibitorhypercholesterolemiaJak/STAT/MCP-1 signalingTGF-beta

Identifiers

PMID32359903
PMCPMC7529741
OpenAlexW3013558186

What OpenQuestion holds

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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.