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Study · Animal study (in vivo) · rat · 2026

8 results

Maternal Kisspeptin-10 Treatment Partially Rescues Fetal and Postnatal Cardiac Programming Disrupted by Maternal Hypothyroidism.

Barbosa EM, Rodrigues NP, Santos BR, Dos Anjos Cordeiro JM, da Silva TQM, Oliveira CL, Santos LC, Cunha MCDSG, Serakides R, Silva JF

Cardiovascular toxicology11 Sept 2026

Summary

Cardiovascular diseases are the leading cause of global mortality and have been associated with alterations in fetal programming. Maternal hypothyroidism (MH) impairs placental function and induces intrauterine growth restriction (IUGR), both of which are risk factors for cardiovascular disease. Kisspeptin-10 (Kp10) has been shown to improve feto-placental development in hypothyroid rats, but its effects on intrauterine cardiac development remain unknown. MH was induced in Wistar rats using propylthiouracil (PTU), and Kp10 administration began on gestational day 8. Offspring hearts were analyzed at fetal day 18 and postnatal days 3 and 21. MH reduced fetal and postnatal body and heart mass, impaired cardiomyocyte proliferation, and dysregulated apoptotic and angiogenic markers. Maternal Kp10 administration enhanced postnatal weight gain, restored cardiomyocyte proliferation and nuclear density, and positively modulated apoptotic (Bax/Bcl2) and angiogenic (Vegf, Ang2, Flk1) pathways. However, it increased redox (8-OHdG) and endoplasmic reticulum (ER) stress (Grp78, Chop) mediators in fetal hearts, while reduced postnatal Chop expression in both sexes. Collectively, these findings demonstrate that maternal hypothyroidism disrupts cardiac development and postnatal cardiac programming, whereas maternal Kp10 administration partially mitigates these effects, highlighting novel mechanisms through which kisspeptin may positively regulate cardiac development.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study8

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In offspring of hypothyroid rats, maternal Kp10 enhanced postnatal weight gain.

    In plain wordsIn rats, giving Kp10 to hypothyroid mothers increased their offspring's weight gain after birth.

    Outcome
    IncreasePostnatal weight gain
    Study

    ratn: not reported in source

    Wistar rats with propylthiouracil-induced maternal hypothyroidism
    Comparator
    Untreated maternal hypothyroidism
    Outcome group
    Body weight · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Maternal Kp10 administration enhanced postnatal weight gain
    2 context sentences
    Summary · context
    MH was induced in Wistar rats using propylthiouracil (PTU), and Kp10 administration began on gestational day 8.
    Summary · context
    Offspring hearts were analyzed at fetal day 18 and postnatal days 3 and 21.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In offspring of hypothyroid rats, maternal Kp10 restored cardiomyocyte proliferation.

    In plain wordsIn rats, giving Kp10 to hypothyroid mothers restored heart cell growth in their offspring.

    Outcome
    IncreaseCardiomyocyte proliferation
    Study

    ratn: not reported in source

    Wistar rats with propylthiouracil-induced maternal hypothyroidism
    Comparator
    Untreated maternal hypothyroidism
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    restored cardiomyocyte proliferation
    2 context sentences
    Summary · context
    MH was induced in Wistar rats using propylthiouracil (PTU), and Kp10 administration began on gestational day 8.
    Summary · context
    Offspring hearts were analyzed at fetal day 18 and postnatal days 3 and 21.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In offspring of hypothyroid rats, maternal Kp10 restored nuclear density of cardiomyocytes.

    In plain wordsIn rats, giving Kp10 to hypothyroid mothers restored the nuclear density of heart cells in their offspring.

    Outcome
    IncreaseCardiomyocyte nuclear density
    Study

    ratn: not reported in source

    Wistar rats with propylthiouracil-induced maternal hypothyroidism
    Comparator
    Untreated maternal hypothyroidism
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    restored cardiomyocyte proliferation and nuclear density
    2 context sentences
    Summary · context
    MH was induced in Wistar rats using propylthiouracil (PTU), and Kp10 administration began on gestational day 8.
    Summary · context
    Offspring hearts were analyzed at fetal day 18 and postnatal days 3 and 21.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In offspring of hypothyroid rats, maternal Kp10 positively modulated the apoptotic pathway (Bax/Bcl2).

    In plain wordsIn rats, giving Kp10 to hypothyroid mothers shifted a cell-death pathway in the offspring's hearts in a favourable direction.

    Outcome
    Direction not reportedApoptotic markers (Bax/Bcl2)
    Study

    ratn: not reported in source

    Wistar rats with propylthiouracil-induced maternal hypothyroidism
    Comparator
    Untreated maternal hypothyroidism
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    positively modulated apoptotic (Bax/Bcl2)
    2 context sentences
    Summary · context
    MH was induced in Wistar rats using propylthiouracil (PTU), and Kp10 administration began on gestational day 8.
    Summary · context
    Offspring hearts were analyzed at fetal day 18 and postnatal days 3 and 21.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In offspring of hypothyroid rats, maternal Kp10 positively modulated the angiogenic pathway (Vegf, Ang2, Flk1).

    In plain wordsIn rats, giving Kp10 to hypothyroid mothers shifted a blood-vessel growth pathway in the offspring's hearts in a favourable direction.

    Outcome
    Direction not reportedAngiogenic markers (Vegf, Ang2, Flk1)
    Study

    ratn: not reported in source

    Wistar rats with propylthiouracil-induced maternal hypothyroidism
    Comparator
    Untreated maternal hypothyroidism
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and angiogenic (Vegf, Ang2, Flk1) pathways
    2 context sentences
    Summary · context
    MH was induced in Wistar rats using propylthiouracil (PTU), and Kp10 administration began on gestational day 8.
    Summary · context
    Offspring hearts were analyzed at fetal day 18 and postnatal days 3 and 21.
  6. 06AnimalAnimal study (in vivo)Safety outcome

    In fetal hearts of hypothyroid rats, maternal Kp10 increased the redox stress mediator 8-OHdG.

    In plain wordsIn rats, giving Kp10 to hypothyroid mothers raised a marker of oxidative stress in the fetal hearts.

    Outcome
    IncreaseRedox stress marker 8-OHdG in fetal hearts
    Study

    ratn: not reported in source

    Wistar rats with propylthiouracil-induced maternal hypothyroidism
    Comparator
    Untreated maternal hypothyroidism
    Outcome group
    Oxidative stress · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    it increased redox (8-OHdG)
    2 context sentences
    Summary · context
    MH was induced in Wistar rats using propylthiouracil (PTU), and Kp10 administration began on gestational day 8.
    Summary · context
    Offspring hearts were analyzed at fetal day 18 and postnatal days 3 and 21.
  7. 07AnimalAnimal study (in vivo)Safety outcome

    In fetal hearts of hypothyroid rats, maternal Kp10 increased the endoplasmic reticulum stress mediators Grp78 and Chop.

    In plain wordsIn rats, giving Kp10 to hypothyroid mothers raised markers of cell stress in the fetal hearts.

    Outcome
    IncreaseER stress mediators (Grp78, Chop) in fetal hearts
    Study

    ratn: not reported in source

    Wistar rats with propylthiouracil-induced maternal hypothyroidism
    Comparator
    Untreated maternal hypothyroidism
    Outcome group
    Oxidative stress · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    endoplasmic reticulum (ER) stress (Grp78, Chop) mediators in fetal hearts
    2 context sentences
    Summary · context
    MH was induced in Wistar rats using propylthiouracil (PTU), and Kp10 administration began on gestational day 8.
    Summary · context
    Offspring hearts were analyzed at fetal day 18 and postnatal days 3 and 21.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In postnatal hearts of hypothyroid rat offspring of both sexes, maternal Kp10 reduced Chop expression.

    In plain wordsIn rats, giving Kp10 to hypothyroid mothers lowered a cell-stress marker in the young offspring's hearts, in both sexes.

    Outcome
    DecreasePostnatal Chop expression
    Study

    ratn: not reported in source

    Wistar rats with propylthiouracil-induced maternal hypothyroidism
    Comparator
    Untreated maternal hypothyroidism
    Outcome group
    Oxidative stress · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    reduced postnatal Chop expression in both sexes.
    2 context sentences
    Summary · context
    MH was induced in Wistar rats using propylthiouracil (PTU), and Kp10 administration began on gestational day 8.
    Summary · context
    Offspring hearts were analyzed at fetal day 18 and postnatal days 3 and 21.

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, 09:43 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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