ArticleInternational journal of molecular sciences2019
High Concentration of C5a-Induced Mitochondria-Dependent Apoptosis in Murine Kidney Endothelial Cells.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 21 citations in OpenAlex.
- Effect of complement 3/5 knockout on renal proteomics landscape after ischemia and reperfusion injury in rats.Physiological reports · 2026Article
- Mitochondria: The Crossroads of Complement Activation and Kidney Injury Progression.International journal of molecular sciences · 2026Review
- Novel interactions between the C5-C5aR1 Axis and IF1: Implications for kidney mitochondrial physiology and ischemia-reperfusion injury.Physiological reports · 2026Article
- Complement in acute kidney injury: a convergent pathogenic pathway in multifactorial renal damage.Frontiers in immunology · 2026Review
- C5a/C5aR regulates Th1/Th2 imbalance in sepsis-associated lung injury by promoting neutrophil activation to increase PAD4 expression.Annals of medicine · 2025Article
- Post-ischemia and reperfusion kidney injury is mitigated in a novel complement 5 knockout rat.Physiological reports · 2025Article
- Exploring Potential Complement Modulation Strategies for Ischemia-Reperfusion Injury in Kidney Transplantation.Antioxidants (Basel, Switzerland) · 2025Review
- C5a Induces Inflammatory Signaling and Apoptosis in PC12 Cells through C5aR-Dependent Signaling: A Potential Mechanism for Adrenal Damage in Sepsis.International journal of molecular sciences · 2024Article
- Double-Edged Sword: Exploring the Mitochondria-Complement Bidirectional Connection in Cellular Response and Disease.Biology · 2024Review
- Membrane potential dynamics of C5a-stimulated neutrophil granulocytes.Pflugers Archiv : European journal of physiology · 2024Article
- Renal improvement and remission in a patient with refractory ANCA-associated vasculitis treated with avacopan.Journal of nephrology · 2023Article
- Therapeutic Potential of Targeting Complement C5a Receptors in Diabetic Kidney Disease.International journal of molecular sciences · 2023Review
- New insight of complement system in the process of vascular calcification.Journal of cellular and molecular medicine · 2023Review
- The Complement Pathway: New Insights into Immunometabolic Signaling in Diabetic Kidney Disease.Antioxidants & redox signaling · 2022Review
- Antioxidants as Therapeutic Agents in Acute Respiratory Distress Syndrome (ARDS) Treatment-From Mice to Men.Biomedicines · 2022Review
- Complement Regulation in Human Tenocytes under the Influence of Anaphylatoxin C5a.International journal of molecular sciences · 2021Article
- Article
- Complement C5 activation promotes type 2 diabetic kidney disease via activating STAT3 pathway and disrupting the gut-kidney axis.Journal of cellular and molecular medicine · 2021Article
- CB11, a novel purine-based PPARɣ ligand, overcomes radio-resistance by regulating ATM signalling and EMT in human non-small-cell lung cancer cells.British journal of cancer · 2020Article
- Natural products and phytochemical nanoformulations targeting mitochondria in oncotherapy: an updated review on resveratrol.Bioscience reports · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with a relapse of idiopathic nephrotic syndrome have significantly increased levels of serum complement component 5a (C5a), and proteinuria has been noted in mice treated with C5a via changes in permeability of kidney endothelial cells (KECs) in established animal models. However, the apoptosis of KECs treated with high concentrations of C5a has also been observed. As mitochondrial damage is known to be important in cell apoptosis, the aim of this study was to examine the association between C5a-induced mouse KEC apoptosis and mitochondrial damage. Mouse KECs were isolated and treated with different concentrations of C5a. Cell viability assays showed that a high-concentration mouse recombinant protein C5a (rmC5a) treatment reduced mouse KEC growth. Cell cycle phase analysis, including apoptosis (sub-G1 phase) showed an increased percentage of the subG1 phase with a high-concentration rmC5a treatment. Cytochrome c and caspase 3/9 activities were significantly induced in the mouse KECs after a high-dose rmC5a (50 ng/mL) treatment, and this was rescued by pretreatment with the C5a receptor (C5aR) inhibitor (W-54011) and N-acetylcysteine (NAC). Reactive oxygen species (ROS) formation was detected in C5a-treated mouse KECs; however, W-54011 or NAC pretreatment inhibited high-dose rmC5a-induced ROS formation and also reduced cytochrome c release, apoptotic cell formation, and apoptotic DNA fragmentation. These factors determined the apoptosis of mouse KECs treated with high-dose C5a through C5aR and subsequently led to apoptosis via ROS regeneration and cytochrome c release. The results showed that high concentrations of C5a induced mouse KEC apoptosis via a C5aR/ROS/mitochondria-dependent pathway. These findings may shed light on the potential mechanism of glomerular sclerosis, a process in idiopathic nephrotic syndrome causing renal function impairment.
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