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Study · Animal study (in vivo) · mouse · 2020

6 results

B7-33, a Functionally Selective Relaxin Receptor 1 Agonist, Attenuates Myocardial Infarction-Related Adverse Cardiac Remodeling in Mice.

Devarakonda T, Mauro AG, Guzman G, Hovsepian S, Cain C, Das A, Praveen P, Hossain MA, Salloum FN

Journal of the American Heart Association16 Apr 2020Cited by 17 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study6

6 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice with ischemia-reperfusion injury, B7‑33 reduced infarct size versus vehicle.

    In plain wordsIn mice with heart ischemia-reperfusion injury, B7‑33 reduced infarct size compared with vehicle.

    Outcome
    DecreaseInfarct size
    Study

    mousen: not reported in source

    Adult male CD1 mouse ischemia-reperfusion injury
    Comparator
    Vehicle
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Measurements

    Infarct size
    21.99%
    B7-33
    Infarct size
    45.32%
    vehicle

    Source sentences

    Summary
    B7-33 significantly reduced infarct size (21.99% versus 45.32%; P=0.02) and preserved fractional shortening (29% versus 23%; P=0.02) compared with vehicle.
    2 context sentences
    Summary · context
    Methods and Results Adult male CD1 mice were subjected to ischemia-reperfusion via ligation of left anterior descending artery for 30 minutes, followed by 24 hours or 7 days of reperfusion.
    Summary · context
    Echocardiography was performed to assess cardiac function, and cardiac tissue was stained to determine infarct size at 24 hours.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with ischemia-reperfusion injury, B7‑33 preserved fractional shortening versus vehicle at 24 hours.

    In plain wordsIn mice with heart injury, B7‑33 preserved heart shortening compared with vehicle at 24 hours.

    Outcome
    IncreaseFractional shortening at 24 hours
    Study

    mousen: not reported in source

    Adult male CD1 mouse ischemia-reperfusion injury
    Comparator
    Vehicle
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Measurements

    Fractional shortening
    29%
    B7-33
    Fractional shortening
    23%
    vehicle

    Source sentences

    Summary
    B7-33 significantly reduced infarct size (21.99% versus 45.32%; P=0.02) and preserved fractional shortening (29% versus 23%; P=0.02) compared with vehicle.
    2 context sentences
    Summary · context
    Methods and Results Adult male CD1 mice were subjected to ischemia-reperfusion via ligation of left anterior descending artery for 30 minutes, followed by 24 hours or 7 days of reperfusion.
    Summary · context
    Echocardiography was performed to assess cardiac function, and cardiac tissue was stained to determine infarct size at 24 hours.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice after myocardial infarction, fractional shortening was higher with B7‑33 than vehicle at 7 days.

    In plain wordsIn mice after heart infarction, B7‑33 preserved heart shortening more than vehicle at 7 days.

    Outcome
    IncreaseFractional shortening at 7 days
    Study

    mousen: not reported in source

    Adult male CD1 mouse ischemia-reperfusion injury
    Comparator
    Vehicle
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Measurements

    Fractional shortening
    29%
    B7-33 at 7 days
    Fractional shortening
    20%
    vehicle at 7 days

    Source sentences

    Summary
    The difference in fractional shortening further increased at 7 days post myocardial infarction (29% versus 20% for B7-33 and vehicle groups, respectively).
    1 context sentence
    Summary · context
    Methods and Results Adult male CD1 mice were subjected to ischemia-reperfusion via ligation of left anterior descending artery for 30 minutes, followed by 24 hours or 7 days of reperfusion.
  4. 04LabIn vitro (cells)Efficacy outcome

    In primary cardiomyocytes with simulated ischemia-reperfusion injury, B7‑33 improved cell survival at 50 and 100 nmol/L.

    In plain wordsIn cells with simulated ischemia-reperfusion injury, B7‑33 improved survival at 50 and 100 nmol/L.

    Outcome
    IncreaseCell survival
    Study

    n: not reported in source

    Primary adult cardiomyocytes subjected to simulated ischemia-reperfusion
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    50 and 100 nmol/LAs given in this study.

    Source sentences

    Summary
    B7-33 (50 and 100 nmol/L) improved cell survival and reduced the expression of GRP78 (glucose regulated protein), an endoplasmic reticulum stress marker.
    1 context sentence
    Summary · context
    In vitro, primary cardiomyocytes were isolated from adult hearts and subjected to simulated ischemia-reperfusion injury (simulated ischemia reoxygenation).
  5. 05LabIn vitro (cells)Mechanism

    In primary cardiomyocytes with simulated ischemia-reperfusion injury, B7‑33 reduced GRP78 expression at 50 and 100 nmol/L.

    In plain wordsIn cells with simulated ischemia-reperfusion injury, B7‑33 reduced the stress marker GRP78 at 50 and 100 nmol/L.

    Outcome
    DecreaseGRP78 expression after simulated ischemia-reperfusion
    Study

    n: not reported in source

    Primary adult cardiomyocytes subjected to simulated ischemia-reperfusion
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    50 and 100 nmol/LAs given in this study.

    Source sentences

    Summary
    B7-33 (50 and 100 nmol/L) improved cell survival and reduced the expression of GRP78 (glucose regulated protein), an endoplasmic reticulum stress marker.
    1 context sentence
    Summary · context
    In vitro, primary cardiomyocytes were isolated from adult hearts and subjected to simulated ischemia-reperfusion injury (simulated ischemia reoxygenation).
  6. 06LabIn vitro (cells)Mechanism

    In primary cardiomyocytes, B7‑33 reduced tunicamycin-induced GRP78 upregulation through an extracellular signal-regulated kinase-dependent mechanism.

    In plain wordsIn cells, B7‑33 reduced tunicamycin-induced GRP78 increases through a mechanism dependent on extracellular signal-regulated kinase.

    Outcome
    DecreaseTunicamycin-induced GRP78 upregulation
    Study

    n: not reported in source

    Primary adult cardiomyocytes challenged with tunicamycin
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    100 nmol/LAs given in this study.

    Source sentences

    Summary
    Subsequently, B7-33 (100 nmol/L) reduced tunicamycin (2.5 μg/mL) induced upregulation of GRP78 in an extracellular signal-regulated kinase 1/2-dependent manner.
    1 context sentence
    Summary · context
    In vitro, primary cardiomyocytes were isolated from adult hearts and subjected to simulated ischemia-reperfusion injury (simulated ischemia reoxygenation).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    22 Oct 2026, 02:25 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 18:59 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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