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Hdac11 promotes idiopathic pulmonary fibrosis through macrophage M2-type polarization and myofibroblast differentiation by inhibiting Parkin-dependent mitophagy

GSE303021 Mus musculus (mouse) RNA-seq (gene expression) 13 samples Submitted 2026/02/27 Platform GPL28330
At a glance

RNA-seq (gene expression) · mouse · 13 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
13 samples: 13 samples, each with a distinct title — no replicated groupsGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
Hdac11 promotes idiopathic pulmonary fibrosis through macrophage M2-type polarization and myofibroblast accumulation by inhibiting Parkin-dependent mitophagyNature communications · 2026
Summary (written by the submitters)
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease in which macrophages play a central role in driving fibrogenesis. In this study, we observed marked upregulation of histone deacetylase 11 (Hdac11) in lung tissues from IPF patients, lung organoid models, and bleomycin‑induced fibrotic mouse lungs, with predominant expression in alveolar macrophages.
Read the full summary ↓
Genetic deletion of Hdac11 or adoptive transfer of Hdac11‑deficient macrophages significantly reduced fibrotic progression. Hdac11 loss impaired M2 macrophage polarization and macrophage‑to‑myofibroblast transition, leading to decreased myofibroblast accumulation and reduced profibrotic gene expression. Mechanistically, Hdac11 directly deacetylates Parkin at lysine 76, promoting its ubiquitination and proteasomal degradation, thereby suppressing Parkin‑mediated mitophagy. Impaired mitophagy resulted in mitochondrial dysfunction that enhanced profibrotic macrophage activation. Pharmacological inhibition of Hdac11 alleviated bleomycin‑induced lung fibrosis. These findings identify Hdac11 as a regulator of Parkin‑dependent mitophagy in macrophages and suggest Hdac11 inhibition as a potential therapeutic strategy for IPF.
Published in
Hdac11 promotes idiopathic pulmonary fibrosis through macrophage M2-type polarization and myofibroblast accumulation by inhibiting Parkin-dependent mitophagy
Nie Y, Xu L, Liu Y et al. · Nature communications 2026 · PMID 41997918 · doi:10.1038/s41467-026-71639-x
This dataset
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE303021_RAW.tar (it can run to tens of gigabytes).

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1293366 and SRA study SRP603159. Searching any of these in the dataset finder brings you back here.

Study design
13 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 13 sample titles: 13 distinct titles with little repetition. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
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