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Study · In vitro (cells) · 2022

7 results

Thymosin β4 Is an Endogenous Iron Chelator and Molecular Switcher of Ferroptosis.

Lachowicz JI, Pichiri G, Piludu M, Fais S, Orrù G, Congiu T, Piras M, Faa G, Fanni D, Dalla Torre G, Lopez X, Chandra K and 8 more

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Szczepski K, Jaremko L, Ghosh M, Emwas AH, Castagnola M, Jaremko M, Hannappel E, Coni P

International journal of molecular sciences4 Jan 2022Cited by 29 (Europe PMC)

PMID35008976 (opens in a new tab)PMCIDPMC8745404 (opens in a new tab)DOI10.3390/ijms23010551 (opens in a new tab)PepBankPUB-35008976
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Summary

Thymosin β4 (Tβ4) was extracted forty years agofrom calf thymus. Since then, it has been identified as a G-actin binding protein involved in blood clotting, tissue regeneration, angiogenesis, and anti-inflammatory processes. Tβ4 has also been implicated in tumor metastasis and neurodegeneration. However, the precise roles and mechanism(s) of action of Tβ4 in these processes remain largely unknown, with the binding of the G-actin protein being insufficient to explain these multi-actions. Here we identify for the first time the important role of Tβ4 mechanism in ferroptosis, an iron-dependent form of cell death, which leads to neurodegeneration and somehow protects cancer cells against cell death. Specifically, we demonstrate four iron2+ and iron3+ binding regions along the peptide and show that the presence of Tβ4 in cell growing medium inhibits erastin and glutamate-induced ferroptosis in the macrophage cell line. Moreover, Tβ4 increases the expression of oxidative stress-related genes, namely BAX, hem oxygenase-1, heat shock protein 70 and thioredoxin reductase 1, which are downregulated during ferroptosis. We state the hypothesis that Tβ4 is an endogenous iron chelator and take part in iron homeostasis in the ferroptosis process. We discuss the literature data of parallel involvement of Tβ4 and ferroptosis in different human pathologies, mainly cancer and neurodegeneration. Our findings confronted with literature data show that controlled Tβ4 release could command on/off switching of ferroptosis and may provide novel therapeutic opportunities in cancer and tissue degeneration pathologies.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study7

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

  1. 01LabIn vitro (cells)Mechanism

    In a macrophage cell line, Tβ4 in the growth medium inhibited erastin-induced ferroptosis.

    In plain wordsIn cells, Tβ4 in the growth medium reduced ferroptosis caused by erastin.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseErastin-induced ferroptosis
    Study

    n: not reported in source

    macrophage cell line
    Outcome group
    Cell viability and death · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    show that the presence of Tβ4 in cell growing medium inhibits erastin and glutamate-induced ferroptosis in the macrophage cell line
  2. 02LabIn vitro (cells)Mechanism

    In a macrophage cell line, Tβ4 in the growth medium inhibited glutamate-induced ferroptosis.

    In plain wordsIn cells, Tβ4 in the growth medium reduced ferroptosis caused by glutamate.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseGlutamate-induced ferroptosis
    Study

    n: not reported in source

    macrophage cell line
    Outcome group
    Cell viability and death · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    show that the presence of Tβ4 in cell growing medium inhibits erastin and glutamate-induced ferroptosis in the macrophage cell line
  3. 03LabIn vitro (cells)Mechanism

    Tβ4 increased the expression of BAX, which is downregulated during ferroptosis.

    In plain wordsIn cells, Tβ4 raised BAX gene expression, which falls during ferroptosis.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseBAX expression
    Study

    n: not reported in source

    macrophage cell line
    Outcome group
    Oxidative stress · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, Tβ4 increases the expression of oxidative stress-related genes, namely BAX, hem oxygenase-1, heat shock protein 70 and thioredoxin reductase 1, which are downregulated during ferroptosis.
  4. 04LabIn vitro (cells)Mechanism

    Tβ4 increased the expression of heme oxygenase-1, which is downregulated during ferroptosis.

    In plain wordsIn cells, Tβ4 raised heme oxygenase-1 gene expression, which falls during ferroptosis.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseHeme oxygenase-1 expression
    Study

    n: not reported in source

    macrophage cell line
    Outcome group
    Oxidative stress · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, Tβ4 increases the expression of oxidative stress-related genes, namely BAX, hem oxygenase-1, heat shock protein 70 and thioredoxin reductase 1, which are downregulated during ferroptosis.
  5. 05LabIn vitro (cells)Mechanism

    Tβ4 increased the expression of heat shock protein 70, which is downregulated during ferroptosis.

    In plain wordsIn cells, Tβ4 raised heat shock protein 70 gene expression, which falls during ferroptosis.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseHeat shock protein 70 expression
    Study

    n: not reported in source

    macrophage cell line
    Outcome group
    Oxidative stress · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, Tβ4 increases the expression of oxidative stress-related genes, namely BAX, hem oxygenase-1, heat shock protein 70 and thioredoxin reductase 1, which are downregulated during ferroptosis.
  6. 06LabIn vitro (cells)Mechanism

    Tβ4 increased the expression of thioredoxin reductase 1, which is downregulated during ferroptosis.

    In plain wordsIn cells, Tβ4 raised thioredoxin reductase 1 gene expression, which falls during ferroptosis.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseThioredoxin reductase 1 expression
    Study

    n: not reported in source

    macrophage cell line
    Outcome group
    Oxidative stress · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, Tβ4 increases the expression of oxidative stress-related genes, namely BAX, hem oxygenase-1, heat shock protein 70 and thioredoxin reductase 1, which are downregulated during ferroptosis.
  7. 07LabIn vitro (cell-free)Mechanism

    In lab tests, Tβ4 had four binding regions for iron 2+ and iron 3+ along the peptide.

    In plain wordsIn lab tests, Tβ4 bound iron at four regions along the peptide.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableIron binding regions on Tβ4
    Study

    n: not reported in source

    Tβ4 peptide
    Outcome group
    Receptor activity and mechanism · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    we demonstrate four iron2+ and iron3+ binding regions along the peptide

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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