GEO series

Pericardial Adipose Tissue Regulates Cardiac Remodeling via Lipolysis-Mediated CD206+ Macrophage Expansion [snRNA-seq]

GSE295609 Homo sapiens (human) Single-nucleus RNA-seq 4 samples Submitted 2026/09/16 Platform GPL24676Platform GPL24247

At a glance

Single-nucleus RNA-seq · human · 4 samples

What it is: Single-nucleus RNA-seqGene activity measured in individual nuclei (used when whole cells are hard to isolate, for example from frozen tissue).
Organism: Homo sapiens (human)
Samples: 4 samples
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.

Summary (written by the submitters)

Obesity is a major risk factor for heart failure (HF). Recent clinical studies suggest an association between pericardial adipose tissue (PeAT) volume and HF, yet the underlying mechanisms remain elusive. Here, we demonstrate that impaired lipolysis in PeAT of obese mice exacerbates cardiac remodeling under pressure overload. High-fat diet (HFD) feeding doubled PeAT volume in mice and accelerated cardiac fibrosis and dysfunction after transverse aortic constriction (TAC).

Read the full summary ↓

PeAT removal prevented the cardiac remodeling in HFD mice, whereas PeAT transplantation from obese mice to lean mice recapitulated the adverse cardiac phenotype. In HFD mice, TGF-β1 was elevated in PeAT with increased downstream SMAD2 activation in adjacent myocardium. Single-nucleus transcriptomics identified CD206+ macrophages as the primary TGF-β1 source in PeAT from both HFD mice and HF patients. Three-dimensional imaging revealed sympathetic denervation in PeAT of obese mice, accompanied by impaired β3-adrenergic receptor-mediated lipolysis signaling, resulting in reduced local free fatty acid (FFA) availability that promoted CD206+ macrophage expansion. Intrapericardial TGF-β1 neutralization ameliorated cardiac remodeling in HFD mice, and further, restoring β3-adrenergic signaling in PeAT increased local FFA levels, suppressed SMAD2 activation in the heart, and improved cardiac function after TAC. These findings establish a mechanistic link between PeAT dysfunction and HF progression in obesity, highlighting PeAT as a potential therapeutic target.

This dataset

Open GSE295609 in finder → Find more RNA-seq datasets →

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.

Series matrix ↓

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 GSE295609_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

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.

Raw reads on ENA ↗

What the files usually look like: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1255463 and SRA study SRP581236. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

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+ 4 more — browse all 4 samples with per-sample file links →

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