ArticleFrontiers in immunology2022
Intracellular Complement Component 3 Attenuated Ischemia-Reperfusion Injury in the Isolated Buffer-Perfused Mouse Heart and Is Associated With Improved Metabolic Homeostasis.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Novel interactions between the C5-C5aR1 Axis and IF1: Implications for kidney mitochondrial physiology and ischemia-reperfusion injury.Physiological reports · 2026Article
- Complosome Activation after Myocardial Infarction in a Murine Model of Permanent LAD Ligation.Stem cell reviews and reports · 2026Article
- Vascular Niches Are the Primary Hotspots in Cardiac Aging.Circulation research · 2025Article
- Complement C3 in panvascular disease: a central integrator of immune signaling and vascular remodeling.Clinical science (London, England : 1979) · 2025Review
- High-fat diet induces pre-eclampsia through dampening cell-autonomous C3 in trophoblasts.Communications biology · 2025Article
- Whole tissue proteomic analyses of cardiac ATTR and AL unveil mechanisms of tissue damage.Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2025Article
- Identification of Potential Biomarkers and Immune Cell Signatures in COVID-19 Myocarditis Through Bioinformatic Analysis.Cardiology research and practice · 2025Article
- Double-Edged Sword: Exploring the Mitochondria-Complement Bidirectional Connection in Cellular Response and Disease.Biology · 2024Review
- Complement: Functions, location and implications.Immunology · 2023Review
- The role of complement C3 in the outcome of regional myocardial infarction.Biochemistry and biophysics reports · 2023Article
- Exosomal HSP90 induced by remote ischemic preconditioning alleviates myocardial ischemia/reperfusion injury by inhibiting complement activation and inflammation.BMC cardiovascular disorders · 2023Article
- Contribution of animal models to the mechanistic understanding of Alternative Pathway and Amplification Loop (AP/AL)-driven Complement-mediated Diseases.Immunological reviews · 2023Review
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The innate immune system is rapidly activated during myocardial infarction and blockade of extracellular complement system reduces infarct size. Intracellular complement, however, appears to be closely linked to metabolic pathways and its role in ischemia-reperfusion injury is unknown and may be different from complement activation in the circulation. The purpose of the present study was to investigate the role of intracellular complement in isolated, retrogradely buffer-perfused hearts and cardiac cells from adult male wild type mice (WT) and from adult male mice with knockout of complement component 3 (C3KO). Main findings: (i) Intracellular C3 protein was expressed in isolated cardiomyocytes and in whole hearts, (ii) after ischemia-reperfusion injury, C3KO hearts had larger infarct size (32 ± 9% in C3KO vs. 22 ± 7% in WT; p=0.008) and impaired post-ischemic relaxation compared to WT hearts, (iii) C3KO cardiomyocytes had lower basal oxidative respiration compared to WT cardiomyocytes, (iv) blocking mTOR decreased Akt phosphorylation in WT, but not in C3KO cardiomyocytes, (v) after ischemia, WT hearts had higher levels of ATP, but lower levels of both reduced and oxidized nicotinamide adenine dinucleotide (NADH and NAD+, respectively) compared to C3KO hearts. Conclusion: intracellular C3 protected the heart against ischemia-reperfusion injury, possibly due to its role in metabolic pathways important for energy production and cell survival.
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