ReviewInternational urology and nephrology2024
Mitophagy in renal interstitial fibrosis.
Review in International urology and nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed.
- Mitochondrial dysfunction-ferroptosis crosstalk drives renal fibrosis in chronic kidney disease.Renal failure · 2026Review
- Mechanistic Insights into Aldose Reductase-Dependent Modulation of Hypoxia-Inducible Factor-1α in Promoting Renal Fibrosis.Cell biochemistry and biophysics · 2026Article
- Mitochondrial Dynamics in Diabetic Kidney Disease: Underlying Mechanisms and Novel Therapeutics.International journal of molecular sciences · 2026Review
- Review
- Knowledge Mapping of Macrophages in Renal Fibrosis: A Bibliometric Analysis from 2014 to 2025.Journal of inflammation research · 2026Review
- Research dynamics and drug treatment of renal fibrosis from a mitochondrial perspective: a historical text data analysis based on bibliometrics.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Inspiring Tactics with the Improvement of Mitophagy and Redox Balance for the Development of Innovative Treatment against Polycystic Kidney Disease.Biomolecules · 2024Review
- Multiple roles of mitochondrial autophagy receptor FUNDC1 in mitochondrial events and kidney disease.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
As a high energy consumption organ, kidney relies on a large number of mitochondria to ensure normal physiological activities. Under specific stimulation, mitophagy and mitochondrial dynamics (fission, fusion) cooperatively regulate mitochondrial quality and participate in many life activities such as energy metabolism, inflammatory response, oxidative stress, cell senescence and death. Mitophagy plays a key role in the progression of acute kidney injury and chronic kidney disease. The early induction of oxidative stress in renal parenchyma, the activation of pro-inflammatory cytokines and TGF-β signal pathway are closely related to renal interstitial fibrosis. Macrophage reprogramming is also considered to be an important participant in the progression of kidney fibrosis. This review summarizes the molecular mechanism of mitochondrial autophagy and its relationship with the pathway of promoting fibrosis, and discusses the possibility of restoring mitophagy balance as a pharmacological target for the treatment of renal interstitial fibrosis, so as to provide new ideas for more efficient anti-fibrosis and delay the progress of chronic kidney disease.
Indexed as
Identifiers
37450241What 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.