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Study · Animal study (in vivo) · rat · 2012

2 results

Mitochondrial permeability transition in the diabetic heart: contributions of thiol redox state and mitochondrial calcium to augmented reperfusion injury.

Sloan RC, Moukdar F, Frasier CR, Patel HD, Bostian PA, Lust RM, Brown DA

Journal of molecular and cellular cardiology3 Mar 2012Cited by 88 (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: Publisher copyright. Results still quote short attributed sentences.

Results from this study2

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In streptozotocin-induced diabetic rats, treatment with MTP-131 improved the resistance of heart mitochondria to permeability transition pore opening.

    In plain wordsIn diabetic rats, MTP-131 made heart mitochondria more resistant to opening of a damaging pore.

    Outcome
    DecreaseMitochondrial PTP opening resistance in diabetic rats
    Study

    ratn: not reported in source

    Mitochondria from hearts of streptozotocin-induced diabetic rats
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Diabetic animals treated with the mitochondria-targeted ROS suppressing peptide MTP-131 also showed improved resistance to PTP opening.
    1 context sentence
    Summary · context
    Hearts from control or streptozotocin-induced diabetic rats were excised for either whole-heart or isolated mitochondria experiments.
  2. 02LabEx vivo tissueEfficacy outcome

    In isolated rat hearts, MTP-131 (1 nM) given at the onset of reperfusion reduced infarct size in both control and diabetic hearts.

    In plain wordsIn lab tests on isolated rat hearts, MTP-131 given at reperfusion reduced the size of the damaged area in healthy and diabetic hearts.

    Outcome
    DecreaseInfarct size after ex vivo ischemia/reperfusion
    Study

    ratn: not reported in source

    Isolated hearts from control and streptozotocin-induced diabetic rats
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    1 nMAs given in this study (rat).

    Measurements

    concentration
    1 nM
    MTP-131

    Source sentences

    Summary
    Administration of the PTP blocker NIM811 (5 μM), MTP-131 (1 nM) or the mitochondrial calcium uniporter blocker minocycline (1 μM) at the onset of reperfusion reduced infarct sizes in both control and diabetic hearts.
    1 context sentence
    Summary · context
    Hearts from control or streptozotocin-induced diabetic rats were excised for either whole-heart or isolated mitochondria experiments.

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

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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