ArticleTheranostics2020
Redox DAPK1 destabilizes Pellino1 to govern inflammation-coupling tubular damage during septic AKI.
Article in Theranostics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 24 citations in OpenAlex.
- Death-associated protein kinase 2 (DAPK2) propagates endoplasmic reticulum stress in macrophages to worsen sepsis through HSPA5-IRE1α axis.Molecular biomedicine · 2026Article
- NTN1 regulates autophagy through the MAP1B/DAPK1 axis to ameliorate acute kidney injuryOpen medicine (Warsaw, Poland) · 2026Article
- DAPK1-positve macrophages facilitate immunosuppressive microenvironment and determine immunotherapy efficacy in colorectal cancer.Journal of translational medicine · 2025Article
- Death-associated protein kinase 1: a double-edged sword in health and disease.Frontiers in immunology · 2025Review
- Article
- Targeting MyD88: Therapeutic mechanisms and potential applications of the specific inhibitor ST2825.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Biology of Pellino1: a potential therapeutic target for inflammation in diseases and cancers.Frontiers in immunology · 2023Review
- The Emerging Roles of Pellino Family in Pattern Recognition Receptor Signaling.Frontiers in immunology · 2022Review
- Interruption of neutrophil extracellular traps formation dictates host defense and tubular HOXA5 stability to augment efficacy of anti-Fn14 therapy against septic AKI.Theranostics · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tubular damage initiated by inflammatory response and ischemic/hypoxic stress is a hallmark of septic acute kidney injury (AKI), albeit the molecular mechanism coupling the two events remains unclear. We investigated the intrinsic nature of tubular damage with respect to inflammatory/hypoxic stress during septic AKI.
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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.