Disrupted macrophage metabolic adaptation and function drive senescence-induced decline in vertebrate regeneration.

ABSTRACT:

Rationale

Senescent cells accumulate with age and contribute to impaired tissue regeneration. Here, we developed a senescence-accelerated zebrafish (SAZ) model, characterized by accelerated senescence-like traits and a significant impairment in caudal fin regeneration.

Methods

To investigate the underlying mechanisms of this regenerative defect, we employed a multifaceted approach. We used transgenic zebrafish lines for 4-D tracking of macrophage subsets during regeneration and performed parabiosis to assess the impact of systemic factors. Then, we isolated macrophages by FACS-sorting for a comprehensive transcriptomic study using RT-qPCR, enabling us to analyze both senescence markers and metabolic markers specifically within SAZ macrophages. Furthermore, we conducted phago

SUBMITTER: Barthelaix A 

PROVIDER: S-EPMC12315812 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature