ArticleJournal of molecular and cellular cardiology2024
Endogenous complement 1q binding protein (C1qbp) regulates mitochondrial permeability transition and post-myocardial infarction remodeling and dysfunction.
Article in Journal of molecular and cellular cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Complement protein C1q induces endothelial apoptosis through C1qBP regulation of mitochondrial function in lung endothelial cells in systemic sclerosis.Molecular medicine (Cambridge, Mass.) · 2026Article
- Cyclophilin D reduces Ca2+ sequestration by complement 1q binding protein.The Biochemical journal · 2025Article
- Trace element-dictated exosome modules and self-adaptive dual-network hydrogel orchestrate diabetic foot regeneration through complement-mitochondria-autophagy circuitry.Military Medical Research · 2025Article
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Authors and funding
5 authors.
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Abstract
The mitochondrial permeability transition (MPT) pore regulates necrotic cell death following diverse cardiac insults. While the componentry of the pore itself remains controversial, Cyclophilin D (CypD) has been well-established as a positive regulator of pore opening. We have previously identified Complement 1q-binding protein (C1qbp) as a novel CypD-interacting molecule and a negative regulator of MPT-dependent cell death in vitro. However, its effects on the MPT pore and sensitivity to cell death in the heart remain untested. We therefore hypothesized that C1qbp would inhibit MPT in cardiac mitochondria and protect cardiac myocytes against cell death in vivo. To investigate the effects of C1qbp in the myocardium we generated gain- and loss-of-function mice. Transgenic C1qbp overexpression resulted in decreased complex protein expression and reduced mitochondrial respiration and ATP production but MPT was unaffected. In contrast, while C1qbp
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