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Study · In vitro (cells) · 2019

8 results

Humanin suppresses receptor activator of nuclear factor-κB ligand-induced osteoclast differentiation via AMP-activated protein kinase activation.

Kang N, Kim KW, Shin DM

The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology26 Aug 2019Cited 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: CC BY-NC. Results still quote short attributed sentences.

Results from this study8

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In bone marrow-derived macrophage cultures, humanin inhibited RANKL-induced osteoclast formation.

    In plain wordsIn cells, humanin reduced the formation of bone-resorbing osteoclasts triggered by RANKL.

    Peptide
    Humanin
    Outcome
    DecreaseRANKL-induced osteoclast formation
    Study

    n: not reported in source

    Bone marrow-derived macrophage (BMM) cultures
    Comparator
    RANKL-induced control
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Our results show that HN inhibited RANKL-induced osteoclast formation and reduced the expression of genes involved in osteoclastogenesis, including nuclear factor of activated T-cells cytoplasmic 1, osteoclast-associated receptor, cathepsin K, and tartrate-resistant acid phosphatase.
    1 context sentence
    Summary · context
    Here, we examined whether HN regulates osteoclastogenesis via AMPK activation using bone marrow-derived macrophage (BMM) cultures.
  2. 02LabIn vitro (cells)Mechanism

    In bone marrow-derived macrophages, humanin reduced expression of nuclear factor of activated T-cells cytoplasmic 1.

    In plain wordsIn cells, humanin reduced the activity of the NFATc1 gene, which drives osteoclast formation.

    Peptide
    Humanin
    Outcome
    DecreaseNFATc1 gene expression
    Study

    n: not reported in source

    Bone marrow-derived macrophage (BMM) cultures
    Comparator
    RANKL-induced control
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Our results show that HN inhibited RANKL-induced osteoclast formation and reduced the expression of genes involved in osteoclastogenesis, including nuclear factor of activated T-cells cytoplasmic 1, osteoclast-associated receptor, cathepsin K, and tartrate-resistant acid phosphatase.
    1 context sentence
    Summary · context
    Here, we examined whether HN regulates osteoclastogenesis via AMPK activation using bone marrow-derived macrophage (BMM) cultures.
  3. 03LabIn vitro (cells)Mechanism

    In bone marrow-derived macrophages, humanin reduced expression of osteoclast-associated receptor.

    In plain wordsIn cells, humanin reduced the activity of the osteoclast-associated receptor gene.

    Peptide
    Humanin
    Outcome
    DecreaseOsteoclast-associated receptor gene expression
    Study

    n: not reported in source

    Bone marrow-derived macrophage (BMM) cultures
    Comparator
    RANKL-induced control
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Our results show that HN inhibited RANKL-induced osteoclast formation and reduced the expression of genes involved in osteoclastogenesis, including nuclear factor of activated T-cells cytoplasmic 1, osteoclast-associated receptor, cathepsin K, and tartrate-resistant acid phosphatase.
    1 context sentence
    Summary · context
    Here, we examined whether HN regulates osteoclastogenesis via AMPK activation using bone marrow-derived macrophage (BMM) cultures.
  4. 04LabIn vitro (cells)Mechanism

    In bone marrow-derived macrophages, humanin reduced expression of cathepsin K.

    In plain wordsIn cells, humanin reduced the activity of the cathepsin K gene.

    Peptide
    Humanin
    Outcome
    DecreaseCathepsin K gene expression
    Study

    n: not reported in source

    Bone marrow-derived macrophage (BMM) cultures
    Comparator
    RANKL-induced control
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Our results show that HN inhibited RANKL-induced osteoclast formation and reduced the expression of genes involved in osteoclastogenesis, including nuclear factor of activated T-cells cytoplasmic 1, osteoclast-associated receptor, cathepsin K, and tartrate-resistant acid phosphatase.
    1 context sentence
    Summary · context
    Here, we examined whether HN regulates osteoclastogenesis via AMPK activation using bone marrow-derived macrophage (BMM) cultures.
  5. 05LabIn vitro (cells)Mechanism

    In bone marrow-derived macrophages, humanin reduced expression of tartrate-resistant acid phosphatase.

    In plain wordsIn cells, humanin reduced the activity of the tartrate-resistant acid phosphatase gene.

    Peptide
    Humanin
    Outcome
    DecreaseTartrate-resistant acid phosphatase gene expression
    Study

    n: not reported in source

    Bone marrow-derived macrophage (BMM) cultures
    Comparator
    RANKL-induced control
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Our results show that HN inhibited RANKL-induced osteoclast formation and reduced the expression of genes involved in osteoclastogenesis, including nuclear factor of activated T-cells cytoplasmic 1, osteoclast-associated receptor, cathepsin K, and tartrate-resistant acid phosphatase.
    1 context sentence
    Summary · context
    Here, we examined whether HN regulates osteoclastogenesis via AMPK activation using bone marrow-derived macrophage (BMM) cultures.
  6. 06LabIn vitro (cells)Mechanism

    In bone marrow-derived macrophages, humanin increased levels of phosphorylated AMPK protein.

    In plain wordsIn cells, humanin raised the level of phosphorylated AMPK, an enzyme that limits osteoclast formation.

    Peptide
    Humanin
    Outcome
    IncreasePhosphorylated AMPK protein level
    Study

    n: not reported in source

    Bone marrow-derived macrophage (BMM) cultures
    Comparator
    RANKL-induced control
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    HN increased the levels of phosphorylated AMPK protein; compound C, an AMPK inhibitor, recovered HN-induced osteoclast differentiation.
    1 context sentence
    Summary · context
    Here, we examined whether HN regulates osteoclastogenesis via AMPK activation using bone marrow-derived macrophage (BMM) cultures.
  7. 07LabIn vitro (cells)Mechanism

    In bone marrow-derived macrophages, the AMPK inhibitor compound C recovered osteoclast differentiation that humanin had suppressed.

    In plain wordsIn cells, blocking AMPK with compound C restored osteoclast formation that humanin had reduced.

    Peptide
    Humanin
    Outcome
    Not applicableOsteoclast differentiation with AMPK inhibitor compound C
    Study

    n: not reported in source

    Bone marrow-derived macrophage (BMM) cultures
    Comparator
    Humanin without compound C
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    compound C, an AMPK inhibitor, recovered HN-induced osteoclast differentiation.
    1 context sentence
    Summary · context
    Here, we examined whether HN regulates osteoclastogenesis via AMPK activation using bone marrow-derived macrophage (BMM) cultures.
  8. 08LabIn vitro (cells)Mechanism

    In bone marrow-derived macrophages, humanin significantly decreased RANKL-induced reactive oxygen species.

    In plain wordsIn cells, humanin significantly lowered reactive oxygen species caused by RANKL.

    Peptide
    Humanin
    Outcome
    DecreaseRANKL-induced reactive oxygen species
    Study

    n: not reported in source

    Bone marrow-derived macrophage (BMM) cultures
    Comparator
    RANKL-induced control
    Outcome group
    Inflammation markers · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, we found that HN significantly decreased the levels of RANKL-induced reactive oxygen species in BMMs.
    1 context sentence
    Summary · context
    Here, we examined whether HN regulates osteoclastogenesis via AMPK activation using bone marrow-derived macrophage (BMM) cultures.

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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