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Frontiers in Cell and Developmental Biology

A protein reduced dialysis-related tissue scarring in mice

In a dialysis mouse model, the protein SIRT3 also suppressed immune cell senescence, a state in which cells stop dividing.

Paper by Funing Wang, Xiaoqian Chen, Hong Deng et al.

Abdominal lining with dense scar fibers beside smoother tissue, surrounded by enlarged damaged immune cells, smaller healthy cells, and a laboratory mouse.
Accepted, not yet published: experiments in miceInterventions

Limit: The abstract does not quantify the reduction in scarring

Edited by Boris Djordjevic · AgingResearch.News

Paper
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Researchers studied a peritoneal dialysis mouse model and RAW264.7 macrophages, immune cells grown in the lab. Peritoneal dialysis uses fluid in the abdomen to filter waste. The experiments altered levels of SIRT3, a protein, and tested honokiol, a drug that activates it, in mice.

In macrophages, dialysis fluid lowered SIRT3 levels, alongside damage to mitochondria, the cells’ energy-producing structures, and release of mitochondrial DNA. Markers of senescence also rose. Increasing SIRT3 or activating it reversed these changes, while reducing SIRT3 produced similar changes to dialysis fluid. The authors also reported reduced scarring of the abdominal lining in the mouse model. They attributed the effects to SIRT3 inhibiting the opening of a mitochondrial pore mediated by BNIP3, another protein. This blocked mitochondrial DNA release and suppressed an inflammatory signaling pathway.

Why it matters

The work addresses how mitochondrial damage and senescence-related inflammation are connected to scarring during long-term peritoneal dialysis.

Caveats

These were experiments in mice and cells grown in the lab, not people receiving dialysis. The abstract does not quantify the reduction in scarring.

Where the evidence stands

Honokiol

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

  • 16 independent labs in 8 countries
  • 2 trials
  • Funders: National Natural Science Foundation of China and others
  • 3 of 41 findings with company ties

SIRT3

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

Includes the processes named after it and trials of drugs aimed at it.

  • 124 independent labs in 27 countries
  • 5 findings against
  • Funders: National Natural Science Foundation of China and others
  • 13 of 348 findings with company ties

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The paper

SIRT3 alleviates macrophage senescence and peritoneal fibrosis: a BNIP3-mediated mechanism targeting the mPTP-mtDNA-cGAS axis

Funing Wang, Xiaoqian Chen, Hong Deng et al.

Frontiers in Cell and Developmental Biology, Nov 2, 2026, CC BY, Accepted, not yet published

Journal site

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