Loss of endogenous thymosin β₄ accelerates glomerular disease.

Vasilopoulou E, Kolatsi-Joannou M, Lindenmeyer MT, White KE, Robson MG, Cohen CD, Sebire NJ, Riley PR, Winyard PJ, Long DA

Kidney international26 Aug 2016Cited by 33 (Europe PMC)

PMID27575556PMCIDPMC5073078DOI10.1016/j.kint.2016.06.032PepBankPUB-27575556

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Summary

Glomerular disease is characterized by morphologic changes in podocyte cells accompanied by inflammation and fibrosis. Thymosin β₄ regulates cell morphology, inflammation, and fibrosis in several organs and administration of exogenous thymosin β₄ improves animal models of unilateral ureteral obstruction and diabetic nephropathy. However, the role of endogenous thymosin β₄ in the kidney is unknown. We demonstrate that thymosin β₄ is expressed prominently in podocytes of developing and adult mouse glomeruli. Global loss of thymosin β₄ did not affect healthy glomeruli, but accelerated the severity of immune-mediated nephrotoxic nephritis with worse renal function, periglomerular inflammation, and fibrosis. Lack of thymosin β₄ in nephrotoxic nephritis led to the redistribution of podocytes from the glomerular tuft toward the Bowman capsule suggesting a role for thymosin β₄ in the migration of these cells. Thymosin β₄ knockdown in cultured podocytes also increased migration in a wound-healing assay, accompanied by F-actin rearrangement and increased RhoA activity. We propose that endogenous thymosin β₄ is a modifier of glomerular injury, likely having a protective role acting as a brake to slow disease progression.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study9

No result from this study comes from a test of the peptide.

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

01AnimalEndogenous levelAnimal study (in vivo)Other
Thymosin β4 is expressed prominently in podocytes of developing and adult mouse glomeruli.
In plain wordsIn mice, the body's own thymosin β4 is found mainly in podocyte cells of the kidney filter.
Peptide
Thymosin beta-4 (human)
Outcome
Not applicableTβ4 expression in glomeruli
Study
mousen: not reported in source
Outcome group
Kidney function · Kidney and urinary
Source sentences
Summary
We demonstrate that thymosin β₄ is expressed prominently in podocytes of developing and adult mouse glomeruli.
This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-2757555601

Studies that did not test the peptide alone8

In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Thymosin beta-4 (human).

02AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome
In mice, global loss of thymosin β4 did not affect healthy glomeruli.
In plain wordsIn mice, losing thymosin β4 did not change healthy kidney filters.
Peptide
Thymosin beta-4 (human)
Outcome
No significant changeHealthy glomeruli after global Tβ4 loss
Study
mousen: not reported in source
Outcome group
Kidney function · Kidney and urinary
Source sentences
Summary
Global loss of thymosin β₄ did not affect healthy glomeruli
In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).
Show in the study text Report a problemFND-2757555602
03AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome
In mice with nephrotoxic nephritis, loss of thymosin β4 accelerated disease with worse renal function.
In plain wordsIn mice with kidney inflammation, losing thymosin β4 led to worse kidney function.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseRenal function in nephrotoxic nephritis
Study
mousen: not reported in source
Outcome group
Kidney function · Kidney and urinary
Source sentences
Summary
but accelerated the severity of immune-mediated nephrotoxic nephritis with worse renal function, periglomerular inflammation, and fibrosis.
In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).
Show in the study text Report a problemFND-2757555603
04AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome
In mice with nephrotoxic nephritis, loss of thymosin β4 accelerated disease with worse periglomerular inflammation.
In plain wordsIn mice with kidney inflammation, losing thymosin β4 led to more inflammation around the kidney filters.
Peptide
Thymosin beta-4 (human)
Outcome
IncreasePeriglomerular inflammation in nephrotoxic nephritis
Study
mousen: not reported in source
Outcome group
Inflammation markers · Kidney and urinary
Source sentences
Summary
but accelerated the severity of immune-mediated nephrotoxic nephritis with worse renal function, periglomerular inflammation, and fibrosis.
In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).
Show in the study text Report a problemFND-2757555604
05AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome
In mice with nephrotoxic nephritis, loss of thymosin β4 accelerated disease with worse fibrosis.
In plain wordsIn mice with kidney inflammation, losing thymosin β4 led to more scarring in the kidney.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseFibrosis in nephrotoxic nephritis
Study
mousen: not reported in source
Outcome group
Kidney function · Kidney and urinary
Source sentences
Summary
but accelerated the severity of immune-mediated nephrotoxic nephritis with worse renal function, periglomerular inflammation, and fibrosis.
In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).
Show in the study text Report a problemFND-2757555605
06AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Mechanism
In mice with nephrotoxic nephritis, lack of thymosin β4 redistributed podocytes from the glomerular tuft toward the Bowman capsule.
In plain wordsIn mice with kidney inflammation, lacking thymosin β4 moved podocyte cells away from the kidney filter toward its outer capsule.
Peptide
Thymosin beta-4 (human)
Outcome
MixedPodocyte distribution in nephrotoxic nephritis
Study
mousen: not reported in source
Outcome group
Kidney function · Kidney and urinary
Source sentences
Summary
Lack of thymosin β₄ in nephrotoxic nephritis led to the redistribution of podocytes from the glomerular tuft toward the Bowman capsule suggesting a role for thymosin β₄ in the migration of these cells.
In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).
Show in the study text Report a problemFND-2757555606
07LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
Thymosin β4 knockdown in cultured podocytes increased migration in a wound-healing assay.
In plain wordsIn cultured podocytes, lowering thymosin β4 made the cells move more in a wound-healing test.
Peptide
Thymosin beta-4 (human)
Outcome
IncreasePodocyte migration after Tβ4 knockdown
Study
n: not reported in source
Cultured podocytes, wound-healing assay
Outcome group
Kidney function · Kidney and urinary
Source sentences
Summary
Thymosin β₄ knockdown in cultured podocytes also increased migration in a wound-healing assay
In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).
Show in the study text Report a problemFND-2757555607
08LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
Thymosin β4 knockdown in cultured podocytes was accompanied by F-actin rearrangement.
In plain wordsIn cultured podocytes, lowering thymosin β4 came with a change in the cell's actin fibre structure.
Peptide
Thymosin beta-4 (human)
Outcome
MixedF-actin rearrangement after Tβ4 knockdown
Study
n: not reported in source
Cultured podocytes
Outcome group
Receptor activity and mechanism · Kidney and urinary
Source sentences
Summary
Thymosin β₄ knockdown in cultured podocytes also increased migration in a wound-healing assay, accompanied by F-actin rearrangement and increased RhoA activity.
In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).
Show in the study text Report a problemFND-2757555608
09LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
Thymosin β4 knockdown in cultured podocytes was accompanied by increased RhoA activity.
In plain wordsIn cultured podocytes, lowering thymosin β4 came with higher RhoA activity.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseRhoA activity after Tβ4 knockdown
Study
n: not reported in source
Cultured podocytes
Outcome group
Receptor activity and mechanism · Kidney and urinary
Source sentences
Summary
Thymosin β₄ knockdown in cultured podocytes also increased migration in a wound-healing assay, accompanied by F-actin rearrangement and increased RhoA activity.
In this study, Thymosin beta-4 (human) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Thymosin beta-4 (human).
Show in the study text Report a problemFND-2757555609

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.

Version 2Current
13 Oct 2026, 01:52 UTC
Study results updated
Version 1
12 Oct 2026, 18:17 UTC
First added · source update from Europe PMC

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