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Study · Animal study (in vivo) · mouse · 2019

6 results

Thymosin β4 promotes autophagy and repair via HIF-1α stabilization in chronic granulomatous disease.

Renga G, Oikonomou V, Moretti S, Stincardini C, Bellet MM, Pariano M, Bartoli A, Brancorsini S, Mosci P, Finocchi A, Rossi P, Costantini C, Garaci E, Goldstein AL, Romani L

Life science alliance12 Nov 2019Cited by 14 (Europe PMC)

Summary

Chronic granulomatous disease (CGD) is a genetic disorder of the NADPH oxidase characterized by increased susceptibility to infections and hyperinflammation associated with defective autophagy and increased inflammasome activation. Herein, we demonstrate that thymosin β4 (Tβ4), a g-actin sequestering peptide with multiple and diverse intracellular and extracellular activities affecting inflammation, wound healing, fibrosis, and tissue regeneration, promoted in human and murine cells noncanonical autophagy, a form of autophagy associated with phagocytosis and limited inflammation via the death-associated protein kinase 1. We further show that the hypoxia inducible factor-1 (HIF-1)α was underexpressed in CGD but normalized by Tβ4 to promote autophagy and up-regulate genes involved in mucosal barrier protection. Accordingly, inflammation and granuloma formation were impaired and survival increased in CGD mice with colitis or aspergillosis upon Tβ4 treatment or HIF-1α stabilization. Thus, the promotion of endogenous pathways of inflammation resolution through HIF-1α stabilization is druggable in CGD by Tβ4.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study6

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In CGD mice with colitis or aspergillosis, inflammation was impaired upon Tβ4 treatment or HIF-1α stabilization.

    In plain wordsIn mice with chronic granulomatous disease, thymosin beta‑4 treatment or HIF-1α stabilization reduced inflammation.

    Outcome
    DecreaseInflammation
    Study

    mousen: not reported in source

    CGD mice with colitis or aspergillosis
    Comparator
    Untreated CGD
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Accordingly, inflammation and granuloma formation were impaired and survival increased in CGD mice with colitis or aspergillosis upon Tβ4 treatment or HIF-1α stabilization.
    1 context sentence
    Summary · context
    Chronic granulomatous disease (CGD) is a genetic disorder of the NADPH oxidase characterized by increased susceptibility to infections and hyperinflammation associated with defective autophagy and increased inflammasome activation.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In CGD mice with colitis or aspergillosis, granuloma formation was impaired upon Tβ4 treatment or HIF-1α stabilization.

    In plain wordsIn mice with chronic granulomatous disease, thymosin beta‑4 treatment or HIF-1α stabilization reduced granuloma formation.

    Outcome
    DecreaseGranuloma formation
    Study

    mousen: not reported in source

    CGD mice with colitis or aspergillosis
    Comparator
    Untreated CGD
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Accordingly, inflammation and granuloma formation were impaired and survival increased in CGD mice with colitis or aspergillosis upon Tβ4 treatment or HIF-1α stabilization.
    1 context sentence
    Summary · context
    Chronic granulomatous disease (CGD) is a genetic disorder of the NADPH oxidase characterized by increased susceptibility to infections and hyperinflammation associated with defective autophagy and increased inflammasome activation.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In CGD mice with colitis or aspergillosis, survival increased upon Tβ4 treatment or HIF-1α stabilization.

    In plain wordsIn mice with chronic granulomatous disease, thymosin beta‑4 treatment or HIF-1α stabilization increased survival.

    Outcome
    IncreaseSurvival
    Study

    mousen: not reported in source

    CGD mice with colitis or aspergillosis
    Comparator
    Untreated CGD
    Outcome group
    Mortality · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Accordingly, inflammation and granuloma formation were impaired and survival increased in CGD mice with colitis or aspergillosis upon Tβ4 treatment or HIF-1α stabilization.
    1 context sentence
    Summary · context
    Chronic granulomatous disease (CGD) is a genetic disorder of the NADPH oxidase characterized by increased susceptibility to infections and hyperinflammation associated with defective autophagy and increased inflammasome activation.
  4. 04LabIn vitro (cells)Mechanism

    In human and murine cells, thymosin β4 promoted noncanonical autophagy via death-associated protein kinase 1.

    In plain wordsIn human and mouse cells, thymosin beta‑4 promoted a form of cell self-cleaning linked to limited inflammation.

    Outcome
    IncreaseNoncanonical autophagy
    Study

    human and mousen: not reported in source

    Human and murine cells (chronic granulomatous disease)
    Comparator
    Untreated CGD
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Herein, we demonstrate that thymosin β4 (Tβ4), a g-actin sequestering peptide with multiple and diverse intracellular and extracellular activities affecting inflammation, wound healing, fibrosis, and tissue regeneration, promoted in human and murine cells noncanonical autophagy, a form of autophagy associated with phagocytosis and limited inflammation via the death-associated protein kinase 1.
    1 context sentence
    Summary · context
    Chronic granulomatous disease (CGD) is a genetic disorder of the NADPH oxidase characterized by increased susceptibility to infections and hyperinflammation associated with defective autophagy and increased inflammasome activation.
  5. 05LabIn vitro (cells)Mechanism

    HIF-1α was underexpressed in chronic granulomatous disease and was normalized by Tβ4.

    In plain wordsIn lab cells from chronic granulomatous disease, thymosin beta‑4 brought the low level of the protein HIF-1α back to normal.

    Outcome
    IncreaseHIF-1α expression in CGD
    Study

    n: not reported in source

    Comparator
    Untreated CGD
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    the hypoxia inducible factor-1 (HIF-1)α was underexpressed in CGD but normalized by Tβ4
    1 context sentence
    Summary · context
    Chronic granulomatous disease (CGD) is a genetic disorder of the NADPH oxidase characterized by increased susceptibility to infections and hyperinflammation associated with defective autophagy and increased inflammasome activation.
  6. 06LabIn vitro (cells)Mechanism

    In chronic granulomatous disease, Tβ4 normalization of HIF-1α was linked to up-regulation of genes involved in mucosal barrier protection.

    In plain wordsIn lab cells from chronic granulomatous disease, thymosin beta‑4 raised the activity of genes that protect the gut lining.

    Outcome
    IncreaseGenes involved in mucosal barrier protection
    Study

    n: not reported in source

    Comparator
    Untreated CGD
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    to promote autophagy and up-regulate genes involved in mucosal barrier protection.
    1 context sentence
    Summary · context
    Chronic granulomatous disease (CGD) is a genetic disorder of the NADPH oxidase characterized by increased susceptibility to infections and hyperinflammation associated with defective autophagy and increased inflammasome activation.

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, 01:52 UTC

    Study results updated

  2. Version 1

    12 Oct 2026, 18:17 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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