ReviewFrontiers in immunology2021
Role of Damage-Associated Molecular Patterns in Septic Acute Kidney Injury, From Injury to Recovery.
Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 46 citations in OpenAlex.
- Apoptotic Bodies in Kidney Disease: Orchestrators of Inflammation, Fibrosis, and Repair.Journal of the American Society of Nephrology : JASN · 2026Review
- Recent advances in stimuli-responsive nanomaterials for the treatment of acute kidney injury.Journal of nanobiotechnology · 2026Review
- NINJ1 ubiquitination by TRIM72 protects against plasma membrane rupture and AKI-CKD progression.Cell death and differentiation · 2026Article
- Acute kidney injury following household pyrethroid aerosol insecticide exposure: a case report and literature review.Frontiers in medicine · 2026Article
- S100A12 drives inflammatory and metabolic reprogramming in sepsis-associated acute kidney injury.Frontiers in molecular biosciences · 2026Review
- Tanshinone IIA prevents septicemia acute kidney injury via regulating the DUSP10/JNK/P38/NLRP3 pathway.American journal of translational research · 2026Article
- Mitophagy in kidney and lung epithelial cells: molecular mechanisms, crosstalk, and therapeutic interventions.Frontiers in physiology · 2026Review
- High-mobility group box 1 protein, histone H3 and histone H4 are not associated with peripheral hypoperfusion in sepsis: a retrospective cohort study.Einstein (Sao Paulo, Brazil) · 2026Article
- Sepsis and heatstroke: overlapping and distinct mechanisms of systemic inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Damage-associated molecular patterns (DAMPs) in diseases: implications for therapy.Molecular biomedicine · 2025Review
- COVID-19 associated acute kidney injury.Infectious diseases & immunity · 2025Review
- Harnessing the power of nanoagents in acute kidney injury: A versatile platform for imaging and treatment.Coordination chemistry reviews · 2025Article
- Advances in Nano-Immunomodulatory Systems for the Treatment of Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Targeting the epigenetic regulation of ferroptosis: a potential therapeutic approach for sepsis-associated acute kidney injury.Clinical epigenetics · 2025Review
- Biomimetic optimization of silicone breast implant integration: insights into wound healing and the foreign body response.Frontiers in bioengineering and biotechnology · 2025Review
- High-mobility group box 1 in acute kidney injury.Frontiers in pharmacology · 2025Review
- The key players of inflammasomes and pyroptosis in sepsis-induced pathogenesis and organ dysfunction.Frontiers in pharmacology · 2025Review
- Article
- Research progress on damage-associated molecular patterns in acute kidney injury.Frontiers in immunology · 2025Review
- Magnetic vagus nerve stimulation ameliorates contrast-induced acute kidney injury by circulating plasma exosomal miR-365-3p.Journal of nanobiotechnology · 2024Article
Corrections and comments
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Authors and funding
5 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Damage-associated molecular patterns (DAMPs) are a group of immunostimulatory molecules, which take part in inflammatory response after tissue injury. Kidney-specific DAMPs include Tamm-Horsfall glycoprotein, crystals, and uromodulin, released by tubular damage for example. Non-kidney-specific DAMPs include intracellular particles such as nucleus [histones, high-mobility group box 1 protein (HMGB1)] and cytosol parts. DAMPs trigger innate immunity by activating the NRLP3 inflammasome, G-protein coupled class receptors or the Toll-like receptor. Tubular necrosis leads to acute kidney injury (AKI) in either septic, ischemic or toxic conditions. Tubular necrosis releases DAMPs such as histones and HMGB1 and increases vascular permeability, which perpetuates shock and hypoperfusion via Toll Like Receptors. In acute tubular necrosis, intracellular abundance of NADPH may explain a chain reaction where necrosis spreads from cell to cell. The nature AKI in intensive care units does not have preclinical models that meet a variation of blood perfusion or a variation of glomerular filtration within hours before catecholamine infusion. However, the dampening of several DAMPs in AKI could provide organ protection. Research should be focused on the numerous pathophysiological pathways to identify the relative contribution to renal dysfunction. The therapeutic perspectives could be strategies to suppress side effect of DAMPs and to promote renal function regeneration.
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