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Study · In vitro (cells) · 2021

12 results

Effect of anti-hyperglycemic drugs on endoplasmic reticulum (ER) stress in human coronary artery endothelial cells.

Kapadia P, Bikkina P, Landicho MA, Parekh S, Haas MJ, Mooradian AD

European journal of pharmacology9 Jun 2021Cited by 37 (Europe PMC)

PMID34116042 (opens in a new tab)DOI10.1016/j.ejphar.2021.174249 (opens in a new tab)PepBankPUB-34116042
Publisher pagePubMedAsk about this study
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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 study12

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

  1. 01LabIn vitro (cells)Mechanism

    In human coronary endothelial cells, liraglutide reduced tunicamycin-induced ER stress.

    In plain wordsIn cells, liraglutide reduced ER stress caused by tunicamycin.

    Peptide
    Liraglutide
    Outcome
    DecreaseTunicamycin-induced ER stress
    Study

    humann: not reported in source

    Human coronary artery endothelial cells
    Comparator
    Tunicamycin challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Metformin, GLP-1 receptor agonists (GLP-1, exendin 4, liraglutide, albiglutide, and lixisenatide) and SGLT-2 inhibitors (canagliflozin, dapagliflozin, and empagliflozin) were the only anti-hyperglycemic drugs screened that reduced ER stress caused by pharmacological (tunicamycin) or hyperglycemic conditions.
    2 context sentences
    Summary · context
    ER stress was measured in human coronary artery endothelial cells (HCAEC) either treated with tunicamycin (TM) or cultured in hyperglycemic conditions (27.5 mM dextrose).
    Summary · context
    The ER stress was measured with the secreted alkaline phosphatase (ES-TRAP) assay.
  2. 02LabIn vitro (cells)Mechanism

    In human coronary endothelial cells, liraglutide reduced hyperglycemia-induced ER stress.

    In plain wordsIn cells, liraglutide reduced ER stress caused by high glucose.

    Peptide
    Liraglutide
    Outcome
    DecreaseHyperglycemia-induced ER stress
    Study

    humann: not reported in source

    Human coronary artery endothelial cells
    Comparator
    Hyperglycemic conditions
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Metformin, GLP-1 receptor agonists (GLP-1, exendin 4, liraglutide, albiglutide, and lixisenatide) and SGLT-2 inhibitors (canagliflozin, dapagliflozin, and empagliflozin) were the only anti-hyperglycemic drugs screened that reduced ER stress caused by pharmacological (tunicamycin) or hyperglycemic conditions.
    2 context sentences
    Summary · context
    ER stress was measured in human coronary artery endothelial cells (HCAEC) either treated with tunicamycin (TM) or cultured in hyperglycemic conditions (27.5 mM dextrose).
    Summary · context
    The ER stress was measured with the secreted alkaline phosphatase (ES-TRAP) assay.
  3. 03LabIn vitro (cells)Mechanism

    In human coronary endothelial cells, lixisenatide reduced tunicamycin-induced ER stress.

    In plain wordsIn cells, lixisenatide reduced ER stress caused by tunicamycin.

    Peptide
    Lixisenatide
    Outcome
    DecreaseTunicamycin-induced ER stress
    Study

    humann: not reported in source

    Human coronary artery endothelial cells
    Comparator
    Tunicamycin challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Metformin, GLP-1 receptor agonists (GLP-1, exendin 4, liraglutide, albiglutide, and lixisenatide) and SGLT-2 inhibitors (canagliflozin, dapagliflozin, and empagliflozin) were the only anti-hyperglycemic drugs screened that reduced ER stress caused by pharmacological (tunicamycin) or hyperglycemic conditions.
    2 context sentences
    Summary · context
    ER stress was measured in human coronary artery endothelial cells (HCAEC) either treated with tunicamycin (TM) or cultured in hyperglycemic conditions (27.5 mM dextrose).
    Summary · context
    The ER stress was measured with the secreted alkaline phosphatase (ES-TRAP) assay.
  4. 04LabIn vitro (cells)Mechanism

    In human coronary endothelial cells, lixisenatide reduced hyperglycemia-induced ER stress.

    In plain wordsIn cells, lixisenatide reduced ER stress caused by high glucose.

    Peptide
    Lixisenatide
    Outcome
    DecreaseHyperglycemia-induced ER stress
    Study

    humann: not reported in source

    Human coronary artery endothelial cells
    Comparator
    Hyperglycemic conditions
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Metformin, GLP-1 receptor agonists (GLP-1, exendin 4, liraglutide, albiglutide, and lixisenatide) and SGLT-2 inhibitors (canagliflozin, dapagliflozin, and empagliflozin) were the only anti-hyperglycemic drugs screened that reduced ER stress caused by pharmacological (tunicamycin) or hyperglycemic conditions.
    2 context sentences
    Summary · context
    ER stress was measured in human coronary artery endothelial cells (HCAEC) either treated with tunicamycin (TM) or cultured in hyperglycemic conditions (27.5 mM dextrose).
    Summary · context
    The ER stress was measured with the secreted alkaline phosphatase (ES-TRAP) assay.
  5. 05LabIn vitro (cells)Mechanism

    In human coronary endothelial cells, liraglutide suppressed high-dextrose-induced IRE1α phosphorylation.

    In plain wordsIn cells, liraglutide reduced IRE1α phosphorylation compared with the high-glucose challenge alone.

    Peptide
    Liraglutide
    Outcome
    DecreaseIRE1α phosphorylation
    Study

    humann: not reported in source

    Human coronary artery endothelial cells
    Comparator
    High-dextrose challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    High-dextrose and TM increased IRE1α and PERK phosphorylation and ATF6 and GRP78 expression, while treatment with metformin, liraglutide (a GLP-1 receptor agonist) and dapagliflozin (a SGLT-2 inhibitor), suppressed IRE1α and PERK phosphorylation as well as ATF6 and GRP78 expression.
    2 context sentences
    Summary · context
    ER stress was measured in human coronary artery endothelial cells (HCAEC) either treated with tunicamycin (TM) or cultured in hyperglycemic conditions (27.5 mM dextrose).
    Summary · context
    The ER stress was measured with the secreted alkaline phosphatase (ES-TRAP) assay.
  6. 06LabIn vitro (cells)Mechanism

    In human coronary endothelial cells, liraglutide suppressed high-dextrose-induced PERK phosphorylation.

    In plain wordsIn cells, liraglutide reduced PERK phosphorylation compared with the high-glucose challenge alone.

    Peptide
    Liraglutide
    Outcome
    DecreasePERK phosphorylation
    Study

    humann: not reported in source

    Human coronary artery endothelial cells
    Comparator
    High-dextrose challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    High-dextrose and TM increased IRE1α and PERK phosphorylation and ATF6 and GRP78 expression, while treatment with metformin, liraglutide (a GLP-1 receptor agonist) and dapagliflozin (a SGLT-2 inhibitor), suppressed IRE1α and PERK phosphorylation as well as ATF6 and GRP78 expression.
    2 context sentences
    Summary · context
    ER stress was measured in human coronary artery endothelial cells (HCAEC) either treated with tunicamycin (TM) or cultured in hyperglycemic conditions (27.5 mM dextrose).
    Summary · context
    The ER stress was measured with the secreted alkaline phosphatase (ES-TRAP) assay.
  7. 07LabIn vitro (cells)Mechanism

    In human coronary endothelial cells, liraglutide suppressed high-dextrose-induced ATF6 expression.

    In plain wordsIn cells, liraglutide reduced ATF6 expression compared with the high-glucose challenge alone.

    Peptide
    Liraglutide
    Outcome
    DecreaseATF6 expression
    Study

    humann: not reported in source

    Human coronary artery endothelial cells
    Comparator
    High-dextrose challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    High-dextrose and TM increased IRE1α and PERK phosphorylation and ATF6 and GRP78 expression, while treatment with metformin, liraglutide (a GLP-1 receptor agonist) and dapagliflozin (a SGLT-2 inhibitor), suppressed IRE1α and PERK phosphorylation as well as ATF6 and GRP78 expression.
    2 context sentences
    Summary · context
    ER stress was measured in human coronary artery endothelial cells (HCAEC) either treated with tunicamycin (TM) or cultured in hyperglycemic conditions (27.5 mM dextrose).
    Summary · context
    The ER stress was measured with the secreted alkaline phosphatase (ES-TRAP) assay.
  8. 08LabIn vitro (cells)Mechanism

    In human coronary endothelial cells, liraglutide suppressed high-dextrose-induced GRP78 expression.

    In plain wordsIn cells, liraglutide reduced GRP78 expression compared with the high-glucose challenge alone.

    Peptide
    Liraglutide
    Outcome
    DecreaseGRP78 expression
    Study

    humann: not reported in source

    Human coronary artery endothelial cells
    Comparator
    High-dextrose challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    High-dextrose and TM increased IRE1α and PERK phosphorylation and ATF6 and GRP78 expression, while treatment with metformin, liraglutide (a GLP-1 receptor agonist) and dapagliflozin (a SGLT-2 inhibitor), suppressed IRE1α and PERK phosphorylation as well as ATF6 and GRP78 expression.
    2 context sentences
    Summary · context
    ER stress was measured in human coronary artery endothelial cells (HCAEC) either treated with tunicamycin (TM) or cultured in hyperglycemic conditions (27.5 mM dextrose).
    Summary · context
    The ER stress was measured with the secreted alkaline phosphatase (ES-TRAP) assay.
  9. 09LabIn vitro (cells)Mechanism

    In human coronary endothelial cells, liraglutide suppressed tunicamycin-induced IRE1α phosphorylation.

    In plain wordsIn cells, liraglutide reduced IRE1α phosphorylation compared with the tunicamycin challenge alone.

    Peptide
    Liraglutide
    Outcome
    DecreaseTunicamycin-induced IRE1α phosphorylation
    Study

    humann: not reported in source

    Human coronary artery endothelial cells
    Comparator
    Tunicamycin challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    High-dextrose and TM increased IRE1α and PERK phosphorylation and ATF6 and GRP78 expression, while treatment with metformin, liraglutide (a GLP-1 receptor agonist) and dapagliflozin (a SGLT-2 inhibitor), suppressed IRE1α and PERK phosphorylation as well as ATF6 and GRP78 expression.
    1 context sentence
    Summary · context
    ER stress was measured in human coronary artery endothelial cells (HCAEC) either treated with tunicamycin (TM) or cultured in hyperglycemic conditions (27.5 mM dextrose).
  10. 10LabIn vitro (cells)Mechanism

    In human coronary endothelial cells, liraglutide suppressed tunicamycin-induced PERK phosphorylation.

    In plain wordsIn cells, liraglutide reduced PERK phosphorylation compared with the tunicamycin challenge alone.

    Peptide
    Liraglutide
    Outcome
    DecreaseTunicamycin-induced PERK phosphorylation
    Study

    humann: not reported in source

    Human coronary artery endothelial cells
    Comparator
    Tunicamycin challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    High-dextrose and TM increased IRE1α and PERK phosphorylation and ATF6 and GRP78 expression, while treatment with metformin, liraglutide (a GLP-1 receptor agonist) and dapagliflozin (a SGLT-2 inhibitor), suppressed IRE1α and PERK phosphorylation as well as ATF6 and GRP78 expression.
    1 context sentence
    Summary · context
    ER stress was measured in human coronary artery endothelial cells (HCAEC) either treated with tunicamycin (TM) or cultured in hyperglycemic conditions (27.5 mM dextrose).
  11. 11LabIn vitro (cells)Mechanism

    In human coronary endothelial cells, liraglutide suppressed tunicamycin-induced ATF6 expression.

    In plain wordsIn cells, liraglutide reduced ATF6 expression compared with the tunicamycin challenge alone.

    Peptide
    Liraglutide
    Outcome
    DecreaseTunicamycin-induced ATF6 expression
    Study

    humann: not reported in source

    Human coronary artery endothelial cells
    Comparator
    Tunicamycin challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    High-dextrose and TM increased IRE1α and PERK phosphorylation and ATF6 and GRP78 expression, while treatment with metformin, liraglutide (a GLP-1 receptor agonist) and dapagliflozin (a SGLT-2 inhibitor), suppressed IRE1α and PERK phosphorylation as well as ATF6 and GRP78 expression.
    1 context sentence
    Summary · context
    ER stress was measured in human coronary artery endothelial cells (HCAEC) either treated with tunicamycin (TM) or cultured in hyperglycemic conditions (27.5 mM dextrose).
  12. 12LabIn vitro (cells)Mechanism

    In human coronary endothelial cells, liraglutide suppressed tunicamycin-induced GRP78 expression.

    In plain wordsIn cells, liraglutide reduced GRP78 expression compared with the tunicamycin challenge alone.

    Peptide
    Liraglutide
    Outcome
    DecreaseTunicamycin-induced GRP78 expression
    Study

    humann: not reported in source

    Human coronary artery endothelial cells
    Comparator
    Tunicamycin challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    High-dextrose and TM increased IRE1α and PERK phosphorylation and ATF6 and GRP78 expression, while treatment with metformin, liraglutide (a GLP-1 receptor agonist) and dapagliflozin (a SGLT-2 inhibitor), suppressed IRE1α and PERK phosphorylation as well as ATF6 and GRP78 expression.
    1 context sentence
    Summary · context
    ER stress was measured in human coronary artery endothelial cells (HCAEC) either treated with tunicamycin (TM) or cultured in hyperglycemic conditions (27.5 mM dextrose).

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 3Current

    28 Oct 2026, 02:03 UTC

    Study results updated

  2. Version 2

    27 Oct 2026, 16:36 UTC

    Study data updated · source update from Europe PMC

  3. Version 1

    9 Oct 2026, 03:05 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

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