ArticlePloS one2025
Intracellular accumulation of free cholesterol in macrophages triggers a PARP1 response to DNA damage and PARP1 impairs lipopolysaccharide-induced inflammatory response.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Genomic Stress and DNA Repair During Macrophage Differentiation and Inflammatory Activation.International journal of molecular sciences · 2026Review
- Identification of Mitochondrial Signature Biomarkers and Molecular Mechanisms in Atherosclerotic Tissues and Blood: Combined Single-Cell and Bulk RNA Sequencing Analysis.Molecular neurobiology · 2026Article
- Restoring Firmicutes-Associated Metabolites: A Gut-Brain Axis Approach to Alleviate Neuroinflammation and Oxidative Stress in Intracerebral Hemorrhage.Current microbiology · 2026Article
- Chronic Cholesterol Exposure Disrupts Macrophage Polarization and Cytokine Secretion in a 3D Microenvironment.ACS omega · 2026Article
- Interaction between Poly(ADP-ribose) polymerase-1 and α-synuclein pathology in Parkinson's disease.Frontiers in neuroscience · 2026Review
- Molecular ART in the Atherosclerotic Lesion: ADP-Ribosylation.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
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Authors and funding
6 authors.
Funding
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Abstract
The formation of macrophage (Mφ) foam cells is a hallmark of atherosclerosis, yet how the process of lipid loading can modulate Mφ inflammatory responses by rewiring their intracellular metabolic circuits is not well understood. Our previous studies have shown that the accumulation of oxidized LDL (oxLDL) or free cholesterol in Mφs impaired their inflammatory response by suppressing HIF-1α-mediated glycolysis and upregulating NRF2 antioxidative response. However, it remains unclear if other metabolic processes are also contributory. In this study, we found that the accumulation of free cholesterol, but not oxLDL, in primary murine thioglycolate-elicited peritoneal Mφs (PMφs) enhanced a PARP1-dependent response associated with repair of DNA damage, which was characterized by poly ADP-ribosylation of proteins, phosphorylation of histone 2A.X and consumption of NAD + . Both oxLDL and cholesterol enhanced the PARP1 response after LPS stimulation. Treatment of PMφs with mitoTEMPO, a specific mitochondrial reactive oxygen species (mtROS) scavenger, alleviated mtROS during cholesterol loading, blocked the PARP1 response and partially restored LPS- induced inflammatory gene expression. In contrast to inhibition of PARP1 enzymatic activity, knockdown of PARP1 expression in RAW264.7 Mφs with siRNA elevated LPS-induced inflammatory gene expression. Overall, our study suggests that cholesterol accumulation triggers a PARP1 response to DNA damage in Mφs and that PARP1 inhibits LPS-mediated inflammation through a non-enzymatic function.
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