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Study · Systematic review · 2024

5 results

Evidence that tirzepatide protects against diabetes-related cardiac damages.

Taktaz F, Scisciola L, Fontanella RA, Pesapane A, Ghosh P, Franzese M, Tortorella G, Puocci A, Sommella E, Signoriello G, Olivieri F, Barbieri M, Paolisso G

Cardiovascular diabetology30 Mar 2024Cited by 39 (Europe PMC)

PMID38555463 (opens in a new tab)PMCIDPMC10981817 (opens in a new tab)DOI10.1186/s12933-024-02203-4 (opens in a new tab)PepBankPUB-38555463
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Summary

BackgroundGlucagon-like peptide-1 receptor agonists (GLP-1RAs) are effective antidiabetic drugs with potential cardiovascular benefits. Despite their well-established role in reducing the risk of major adverse cardiovascular events (MACE), their impact on heart failure (HF) remains unclear. Therefore, our study examined the cardioprotective effects of tirzepatide (TZT), a novel glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) receptor agonist.MethodsA three-steps approach was designed: (i) Meta-analysis investigation with the primary objective of assessing major adverse cardiovascular events (MACE) occurrence from major randomized clinical trials.; (ii) TZT effects on a human cardiac AC16 cell line exposed to normal (5 mM) and high (33 mM) glucose concentrations for 7 days. The gene expression and protein levels of primary markers related to cardiac fibrosis, hypertrophy, and calcium modulation were evaluated. (iii) In silico data from bioinformatic analyses for generating an interaction map that delineates the potential mechanism of action of TZT.ResultsMeta-analysis showed a reduced risk for MACE events by TZT therapy (HR was 0.59 (95% CI 0.40-0.79, Heterogeneity: r2 = 0.01, I2 = 23.45%, H2 = 1.31). In the human AC16 cardiac cell line treatment with 100 nM TZT contrasted high glucose (HG) levels increase in the expression of markers associated with fibrosis, hypertrophy, and cell death (p < 0.05 for all investigated markers). Bioinformatics analysis confirmed the interaction between the analyzed markers and the associated pathways found in AC16 cells by which TZT affects apoptosis, fibrosis, and contractility, thus reducing the risk of heart failure.ConclusionOur findings indicate that TZT has beneficial effects on cardiac cells by positively modulating cardiomyocyte death, fibrosis, and hypertrophy in the presence of high glucose concentrations. This suggests that TZT may reduce the risk of diabetes-related cardiac damage, highlighting its potential as a therapeutic option for heart failure management clinical trials. Our study strongly supports the rationale behind the clinical trials currently underway, the results of which will be further investigated to gain insights into the cardiovascular safety and efficacy of TZT.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study5

5 results from studies that gave the peptide. 1 result from people.

  1. 01HumanSystematic reviewEfficacy outcome

    In a meta-analysis of randomized trials, tirzepatide therapy reduced the risk of major adverse cardiovascular events.

    In plain wordsIn a meta-analysis of trials, tirzepatide lowered the risk of major heart events.

    Peptide
    Tirzepatide
    Outcome
    DecreaseRisk of MACE (hazard ratio)
    Study

    n: not reported in source

    Analysis
    Primary
    Outcome group
    Cardiovascular events · Cardiovascular
    Studied dose
    Dose not stated

    Measurements

    HR
    0.59 ratio
    MACE

    Source sentences

    Summary
    Meta-analysis showed a reduced risk for MACE events by TZT therapy (HR was 0.59 (95% CI 0.40-0.79, Heterogeneity: r2 = 0.01, I2 = 23.45%, H2 = 1.31).
    1 context sentence
    Summary · context
    (i) Meta-analysis investigation with the primary objective of assessing major adverse cardiovascular events (MACE) occurrence from major randomized clinical trials.
  2. 02LabIn vitro (cells)Mechanism

    In human AC16 cardiac cells, tirzepatide 100 nM counteracted the high-glucose increase in fibrosis markers.

    In plain wordsIn cells, tirzepatide reduced the rise in scarring markers that high sugar caused in human heart cells.

    Peptide
    Tirzepatide
    Outcome
    DecreaseFibrosis markers under high glucose
    Study

    humann: not reported in source

    AC16 human cardiac cell line
    Comparator
    High glucose (33 mM) without tirzepatide
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    100 nMAs given in this study (human).

    Source sentences

    Summary
    In the human AC16 cardiac cell line treatment with 100 nM TZT contrasted high glucose (HG) levels increase in the expression of markers associated with fibrosis, hypertrophy, and cell death (p < 0.05 for all investigated markers).
    1 context sentence
    Summary · context
    (ii) TZT effects on a human cardiac AC16 cell line exposed to normal (5 mM) and high (33 mM) glucose concentrations for 7 days.
  3. 03LabIn vitro (cells)Mechanism

    In human AC16 cardiac cells, tirzepatide 100 nM counteracted the high-glucose increase in hypertrophy markers.

    In plain wordsIn cells, tirzepatide reduced the rise in cell-enlargement markers that high sugar caused in human heart cells.

    Peptide
    Tirzepatide
    Outcome
    DecreaseHypertrophy markers under high glucose
    Study

    humann: not reported in source

    AC16 human cardiac cell line
    Comparator
    High glucose (33 mM) without tirzepatide
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    100 nMAs given in this study (human).

    Source sentences

    Summary
    In the human AC16 cardiac cell line treatment with 100 nM TZT contrasted high glucose (HG) levels increase in the expression of markers associated with fibrosis, hypertrophy, and cell death (p < 0.05 for all investigated markers).
    1 context sentence
    Summary · context
    (ii) TZT effects on a human cardiac AC16 cell line exposed to normal (5 mM) and high (33 mM) glucose concentrations for 7 days.
  4. 04LabIn vitro (cells)Mechanism

    In human AC16 cardiac cells, tirzepatide 100 nM counteracted the high-glucose increase in cell death markers.

    In plain wordsIn cells, tirzepatide reduced the rise in cell-death markers that high sugar caused in human heart cells.

    Peptide
    Tirzepatide
    Outcome
    DecreaseCell death markers under high glucose
    Study

    humann: not reported in source

    AC16 human cardiac cell line
    Comparator
    High glucose (33 mM) without tirzepatide
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    100 nMAs given in this study (human).

    Source sentences

    Summary
    In the human AC16 cardiac cell line treatment with 100 nM TZT contrasted high glucose (HG) levels increase in the expression of markers associated with fibrosis, hypertrophy, and cell death (p < 0.05 for all investigated markers).
    1 context sentence
    Summary · context
    (ii) TZT effects on a human cardiac AC16 cell line exposed to normal (5 mM) and high (33 mM) glucose concentrations for 7 days.
  5. 05Computer modelIn silicoMechanism

    Bioinformatic analysis linked the measured markers to pathways in AC16 cells through which tirzepatide may affect apoptosis, fibrosis and contractility.

    In plain wordsIn a computer analysis, tirzepatide was linked to heart-cell pathways involved in cell death, scarring and contraction.

    Peptide
    Tirzepatide
    Outcome
    Not applicablePredicted pathways of tirzepatide action (apoptosis, fibrosis, contractility)
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Bioinformatics analysis confirmed the interaction between the analyzed markers and the associated pathways found in AC16 cells by which TZT affects apoptosis, fibrosis, and contractility

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

    9 Oct 2026, 19:08 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:07 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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