ArticleCellular & molecular biology letters2023
Formyl peptide receptor 2 activation by mitochondrial formyl peptides stimulates the neutrophil proinflammatory response via the ERK pathway and exacerbates ischemia-reperfusion injury.
Article in Cellular & molecular biology letters, 2023. 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, 15 citations in OpenAlex.
- Article
- Targeting phenol-soluble modulin α3-driven M1 macrophage polarization and necroptosis mitigates MRSA infection in mice.Nature communications · 2026Article
- Tumor-to-endothelium mitochondrial transfer licenses endothelial cells for CD8bioRxiv : the preprint server for biology · 2026Article
- Chemo-/radiotherapy-induced cardiomyopathy: roles of mitochondria and endoplasmic reticulum.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026Review
- Mitochondria as Inducers of Neutrophil Extracellular Traps.Inflammation · 2026Review
- Neutrophil Killing ofJournal of innate immunity · 2026Article
- Formyl peptide receptor 2: a potential therapeutic target for inflammation-related diseases.Pharmacological reports : PR · 2025Review
- Focusing on Formyl Peptide Receptors after Traumatic Spinal Cord Injury: from Immune Response to Neurogenesis.Neurochemical research · 2025Review
- Immune Landscape in Kidney Transplantation.Journal of inflammation research · 2025Review
- Advances in immunomodulation for organ transplantation: The role of the Annexin A1/FPR axis.Clinics (Sao Paulo, Brazil) · 2025Article
- Inflammatory changes in the choroid plexus following subarachnoid hemorrhage: the role of innate immune receptors and inflammatory molecules.Frontiers in cellular neuroscience · 2024Article
- Mitochondrial dysfunction as a possible trigger of neuroinflammation at post-traumatic stress disorder (PTSD).Frontiers in physiology · 2023Review
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
Abstract
backgroundIschemia-reperfusion injury (IRI) is an inevitable process in renal transplantation that significantly increases the risk of delayed graft function, acute rejection, and even graft loss. Formyl peptide receptor 2 (FPR2) is an important receptor in multiple septic and aseptic injuries, but its functions in kidney IRI are still unclear. This study was designed to reveal the pathological role of FPR2 in kidney IRI and its functional mechanisms.
methodsTo explore the mechanism of FPR2 in kidney IRI, the model rats were sacrificed after IRI surgery. Immunofluorescence, enzyme-linked immunosorbent assays, and western blotting were used to detect differences in the expression of FPR2 and its ligands between the IRI and control groups. WRW
resultsFPR2 was activated mainly by mtFPs during the acute phase of IRI, mediating neutrophil migration and reactive oxygen species production in the rat kidney through the ERK1/2 pathway. FPR2 blockade in the early phase protected rat kidneys from IRI.
conclusionsmtFPs activated FPR2 during the acute phase of IRI and mediated rat kidney injury by activating the migration and reactive oxygen species generation of neutrophils through the ERK1/2 pathway.
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