ArticleFrontiers in immunology2019
TREM1/3 Deficiency Impairs Tissue Repair After Acute Kidney Injury and Mitochondrial Metabolic Flexibility in Tubular Epithelial Cells.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- DNA methylation-mediated memory of obesity in CD4 T lymphocytes perpetuates immune dysregulation.EMBO reports · 2026Article
- TREM1-NLRP3-driven pyroptosis in sepsis-associated acute kidney injury (AKI) with parallel autophagy changes.Scientific reports · 2026Article
- Research Hotspots in Mitochondria-Related Studies for AKI Treatment: A Bibliometric Study.Drug design, development and therapy · 2024Article
- Nanomedicine embraces the treatment and prevention of acute kidney injury to chronic kidney disease transition: evidence, challenges, and opportunities.Burns & trauma · 2024Review
- Effects ofFrontiers in pharmacology · 2024Article
- Targeting TREM1 augments antitumor T cell immunity by inhibiting myeloid-derived suppressor cells and restraining anti-PD-1 resistance.The Journal of clinical investigation · 2023Article
- A diagnostic model for sepsis-induced acute lung injury using a consensus machine learning approach and its therapeutic implications.Journal of translational medicine · 2023Article
- The biology of TREM receptors.Nature reviews. Immunology · 2023Review
- Cellular senescence in ischemia/reperfusion injury.Cell death discovery · 2022Review
- Article
- Extracellular CIRP induces acute kidney injury via endothelial TREM-1.Frontiers in physiology · 2022Article
- Interaction Between Intrinsic Renal Cells and Immune Cells in the Progression of Acute Kidney Injury.Frontiers in medicine · 2022Review
- TREM-1 Modulation Strategies for Sepsis.Frontiers in immunology · 2022Review
- The Role of Mitochondria in Acute Kidney Injury and Chronic Kidney Disease and Its Therapeutic Potential.International journal of molecular sciences · 2021Review
- LncRNA TUG1 regulates the development of ischemia-reperfusion mediated acute kidney injury through miR-494-3p/E-cadherin axis.Journal of inflammation (London, England) · 2021Article
- TREM-1 promoted apoptosis and inhibited autophagy in LPS-treated HK-2 cells through the NF-κB pathway.International journal of medical sciences · 2021Article
- Metabolic Flexibility and Innate Immunity in Renal Ischemia Reperfusion Injury: The Fine Balance Between Adaptive Repair and Tissue Degeneration.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term sequelae of acute kidney injury (AKI) are associated with incomplete recovery of renal function and the development of chronic kidney disease (CKD), which can be mediated by aberrant innate immune activation, mitochondrial pathology, and accumulation of senescent tubular epithelial cells (TECs). Herein, we show that the innate immune receptor Triggering receptor expressed on myeloid cells-1 (TREM-1) links mitochondrial metabolism to tubular epithelial senescence. TREM-1 is expressed by inflammatory and epithelial cells, both players in renal repair after ischemia/reperfusion (IR)-induced AKI. Hence, we subjected WT and TREM1/3 KO mice to different models of renal IR. TREM1/3 KO mice displayed no major differences during the acute phase of injury, but increased mortality was observed in the recovery phase. This detrimental effect was associated with maladaptive repair, characterized by persistent tubular damage, inflammation, fibrosis, and TEC senescence.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.