Mitochondrial Proteomics Data on S100A9-Deficient Macrophages in Liver Fibrosis

A proteomics study investigating the role of S100A9 in macrophage metabolism during liver fibrosis. The dataset, published by Jinfang Liu on figshare in 2026, includes data from bone marrow-derived and peritoneal macrophages in a mouse model. It likely contains measurements related to oxidative phosphorylation, mitochondrial fusion, ATP production, and macrophage polarization markers like CD206.

Use Cases

• Analyze the link between S100A9 deficiency and enhanced oxidative phosphorylation based on mitochondrial proteomics data.
• Investigate macrophage polarization states (M1/M2) based on CD206 expression levels mentioned in the description.
• Model the effect of OXPHOS inhibition on macrophage phenotype using data from oligomycin treatment experiments.
• Study the correlation between myeloid S100A9 deletion and protection against liver injury and fibrogenesis in a mouse model.

Strengths

• Dataset is shared under a specific open license (CC-BY-NC-4.0).
• The description provides a detailed biological context and experimental findings.
• File size is 25.1 KB, indicating a focused and likely manageable dataset.

Limitations

• Row count is unknown, which may limit suitability assessment.
• Column-level documentation is absent; field semantics must be inferred after download.
• The dataset is small (25.1 KB), indicating limited scope.

Provenance

Source

figshare, author Jinfang Liu.

Collection Method

Likely generated from laboratory experiments involving mitochondrial proteomics, flow cytometry, and a mouse model of liver fibrosis.

Freshness

Last updated 2026-04-28 17:04:32; freshness should be verified.