ReviewInternational journal of molecular sciences2016
Autophagy, Innate Immunity and Tissue Repair in Acute Kidney Injury.
Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 111 citations in OpenAlex.
- Construction, evaluation, and applications of renal barrier-on-a-chip system.Bioactive materials · 2026Review
- YOD1 drives acute kidney injury by deubiquitinating Bax and promoting apoptosis in tubular epithelial cells.Theranostics · 2026Article
- Crosstalk between noncoding RNAs and autophagy in renal cell carcinoma: Deciphering molecular pathways and therapeutic prospects.Cancer cell international · 2025Review
- The reciprocal regulation between autophagy and IL-22: implications for immunity and therapy.Clinical and experimental medicine · 2025Review
- Integrin-Linked Kinase (ILK) Promotes Mitochondrial Dysfunction by Decreasing CPT1A Expression in a Folic Acid-Based Model of Kidney Disease.International journal of molecular sciences · 2025Article
- An autopsy case with tubular obstruction by impacted swollen blebs due to ischemic acute kidney injury.BMC nephrology · 2025Article
- Sigma-1 Receptor Rescues Autophagy Through AMPK/mTOR Signaling Pathway in Sepsis-Induced Acute Kidney Injury.International journal of general medicine · 2025Article
- Dietary ProbioticNutrients · 2024Article
- Dihydromyricetin Nanoparticles Alleviate Lipopolysaccharide-Induced Acute Kidney Injury by Decreasing Inflammation and Cell Apoptosis via the TLR4/NF-κB Pathway.Journal of functional biomaterials · 2024Article
- Cell death induced by acute renal injury: a perspective on the contributions of accidental and programmed cell death.American journal of physiology. Renal physiology · 2024Review
- Article
- Annexin-A5 monomer as a membrane repair agent for the treatment of renal ischemia-reperfusion injury.Molecular biology reports · 2024Article
- Atg5 deficiency in macrophages protects against kidney fibrosis via the CCR6-CCL20 axis.Cell communication and signaling : CCS · 2024Article
- Galectin-3 and Autophagy in Renal Acute Tubular Necrosis.International journal of molecular sciences · 2024Article
- Echinococcus granulosus cyst fluid inhibits KDM6B-mediated demethylation of trimethylated histone H3 lysine 27 and interleukin-1β production in macrophages.Parasites & vectors · 2023Article
- The Molecular Mechanism and Therapeutic Application of Autophagy for Urological Disease.International journal of molecular sciences · 2023Review
- Abnormal Lipoproteins Trigger Oxidative Stress-Mediated Apoptosis of Renal Cells in LCAT Deficiency.Antioxidants (Basel, Switzerland) · 2023Article
- The Role of NLRP3 Inflammasome in IgA Nephropathy.Medicina (Kaunas, Lithuania) · 2022Review
- Cinnamaldehyde attenuates kidney senescence and injury through PI3K/Akt pathway-mediated autophagy via downregulating miR-155.Renal failure · 2022Article
- Role of abnormal energy metabolism in the progression of chronic kidney disease and drug intervention.Renal failure · 2022Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Kidney is a vital organ with high energy demands to actively maintain plasma hemodynamics, electrolytes and water homeostasis. Among the nephron segments, the renal tubular epithelium is endowed with high mitochondria density for their function in active transport. Acute kidney injury (AKI) is an important clinical syndrome and a global public health issue with high mortality rate and socioeconomic burden due to lack of effective therapy. AKI results in acute cell death and necrosis of renal tubule epithelial cells accompanied with leakage of tubular fluid and inflammation. The inflammatory immune response triggered by the tubular cell death, mitochondrial damage, associative oxidative stress, and the release of many tissue damage factors have been identified as key elements driving the pathophysiology of AKI. Autophagy, the cellular mechanism that removes damaged organelles via lysosome-mediated degradation, had been proposed to be renoprotective. An in-depth understanding of the intricate interplay between autophagy and innate immune response, and their roles in AKI pathology could lead to novel therapies in AKI. This review addresses the current pathophysiology of AKI in aspects of mitochondrial dysfunction, innate immunity, and molecular mechanisms of autophagy. Recent advances in renal tissue regeneration and potential therapeutic interventions are also discussed.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.