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Study · In vitro (cells) · 2020

5 results

[Gly14]-humanin restores cathepsin D function via FPRL1 and promotes autophagic degradation of Ox-LDL in HUVECs.

Ding Y, Feng Y, Zou Y, Wang F, Liu H, Liu C, Zhang Y

Nutrition, metabolism, and cardiovascular diseases : NMCD25 Jul 2020Cited by 11 (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 study5

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In HUVECs exposed to Ox-LDL, HNG pretreatment reduced lipid and cholesterol aggregation.

    In plain wordsIn human blood vessel cells exposed to oxidized LDL, a humanin analogue reduced fat and cholesterol build-up.

    Peptide
    Humanin
    Outcome
    DecreaseLipid and cholesterol aggregation
    Study

    humann: not reported in source

    HUVECs exposed to Ox-LDL
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    HNG pretreatment reduced lipid and cholesterol aggregation in HUVECs induced by Ox-LDL, increased LC3-II protein level, decreased P62 protein content, and reversed Ox-LDL-induced cathepsin D functional impairment.
  2. 02LabIn vitro (cells)Mechanism

    In HUVECs exposed to Ox-LDL, HNG pretreatment increased LC3-II protein level.

    In plain wordsIn human blood vessel cells exposed to oxidized LDL, a humanin analogue raised an autophagy marker, LC3-II.

    Peptide
    Humanin
    Outcome
    IncreaseLC3-II protein level
    Study

    humann: not reported in source

    HUVECs exposed to Ox-LDL
    Outcome group
    Cell viability and death · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    HNG pretreatment reduced lipid and cholesterol aggregation in HUVECs induced by Ox-LDL, increased LC3-II protein level, decreased P62 protein content, and reversed Ox-LDL-induced cathepsin D functional impairment.
  3. 03LabIn vitro (cells)Mechanism

    In HUVECs exposed to Ox-LDL, HNG pretreatment decreased P62 protein content.

    In plain wordsIn human blood vessel cells exposed to oxidized LDL, a humanin analogue lowered the autophagy marker P62.

    Peptide
    Humanin
    Outcome
    DecreaseP62 protein content
    Study

    humann: not reported in source

    HUVECs exposed to Ox-LDL
    Outcome group
    Cell viability and death · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    HNG pretreatment reduced lipid and cholesterol aggregation in HUVECs induced by Ox-LDL, increased LC3-II protein level, decreased P62 protein content, and reversed Ox-LDL-induced cathepsin D functional impairment.
  4. 04LabIn vitro (cells)Mechanism

    In HUVECs exposed to Ox-LDL, HNG pretreatment reversed the Ox-LDL-induced impairment of cathepsin D function.

    In plain wordsIn human blood vessel cells exposed to oxidized LDL, a humanin analogue reversed the loss of cathepsin D function.

    Peptide
    Humanin
    Outcome
    IncreaseCathepsin D function
    Study

    humann: not reported in source

    HUVECs exposed to Ox-LDL
    Outcome group
    Cell viability and death · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    HNG pretreatment reduced lipid and cholesterol aggregation in HUVECs induced by Ox-LDL, increased LC3-II protein level, decreased P62 protein content, and reversed Ox-LDL-induced cathepsin D functional impairment.
  5. 05LabIn vitro (cells)Mechanism

    In HUVECs, inhibition of the FPRL1 pathway by FPRL1 siRNA or Boc-MLF blocked all protective effects of HNG.

    In plain wordsIn human blood vessel cells, blocking the FPRL1 receptor pathway stopped all protective effects of a humanin analogue.

    Peptide
    Humanin
    Outcome
    Not applicableFPRL1 dependence of HNG effects
    Study

    humann: not reported in source

    HUVECs exposed to Ox-LDL
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Inhibition of the FPRL1 pathway by FPRL1 siRNA or the FPRL1-specific inhibitor Boc-MLF blocked all HNG's protective effects.

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

    13 Oct 2026, 21:44 UTC

    Study results updated

  2. Version 1

    13 Oct 2026, 16:31 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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