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CCL5 promotes angiotensin II-induced cardiac remodeling through regulation of platelet-driven M2 macrophage polarization

GSE285383 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2025/12/10 Platform GPL21103
At a glance

RNA-seq (gene expression) · mouse · 12 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
12 samples: 3 × WT_C vs 3 × WT_A vs 3 × CCL5_KO_C vs 3 × CCL5_KO_AGroups 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
CCL5 promotes angiotensin II-induced cardiac remodeling through regulation of platelet-driven M2 macrophage polarizationTheranostics · 2026
Summary (written by the submitters)
Aims: Platelet activation plays a critical role in the pathogenesis of cardiovascular disease and inflammation, primarily through interactions with macrophages. CCL5, a chemokine stored in platelet α-granules, is released upon platelet activation. The present study determines the specific role of CCL5 in modulating platelet function, platelet-mediated macrophage polarization, and hypertensive cardiac remodelin.
Read the full summary ↓
Conclusion: These findings underscore the detrimental role of CCL5-mediated platelet activation in triggering inflammatory responses and promoting M2 macrophage polarization during hypertensive cardiac remodeling, revealing the molecular mechanism by which CCL5 facilitates platelet-derived TGF-β1 signaling via NF-κB activation. These results elucidate the crosstalk between platelets and macrophages that exacerbates cardiac remodeling and highlight CCL5 as a potential therapeutic target for reducing inflammation and cardiac injury.
Published in
CCL5 promotes angiotensin II-induced cardiac remodeling through regulation of platelet-driven M2 macrophage polarization
Lv S, Zhou M, Li T et al. · Theranostics 2026 · PMID 41346713 · doi:10.7150/thno.112163
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 GSE285383_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 PRJNA1200797 and SRA study SRP553474. Searching any of these in the dataset finder brings you back here.

Study design
3 × WT_C vs 3 × WT_A vs 3 × CCL5_KO_C vs 3 × CCL5_KO_A

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 of them. 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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