ReviewBioMed research international2022
Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy.
Review in BioMed research international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 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
91 citing papers in PubMed.
- Article
- Article
- Baicalin alleviates Trueperella pyogenes-induced endometritis with associated changes in gut microbiota composition.BMC veterinary research · 2026Article
- Molecular mechanisms underlying FCCP-induced mitophagy in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Review
- Neurons Die Not by One Hit, but by Signaling Convergence.Molecular neurobiology · 2026Review
- The role of gut microbiota-mitochondrial crosstalk in kidney disease: a bibliometric analysis.International urology and nephrology · 2026Article
- The crosslink between autophagy and ferroptosis in polycystic ovary syndrome: from synergistic pathogenesis to targeted therapy.Journal of ovarian research · 2026Review
- Exploring Replicative Senescence and Oxidative Stress-Induced Remodelling of Mitochondrial-Associated Membranes in Human Skin Fibroblasts.Biomolecules · 2026Article
- Peroxiredoxin-Mediated Redox Regulation in Neurons: From Neurite Development to Degeneration.Antioxidants (Basel, Switzerland) · 2026Review
- Mechanisms of Mitochondrial Toxicity and Cytotoxicity Caused by Pseudomonas aeruginosa Pyocyanin in Human Nasal Epithelial Cells.International forum of allergy & rhinology · 2026Article
- Transport Time Does Not Substantially Alter RNA Expression in Human Ovarian Tissue After Standardized Slow-Freezing for Fertility Preservation.Journal of clinical medicine · 2026Article
- [Ophiopogonin D alleviates doxorubicin-induced myocardial hypertrophy in mice by activating the β-catenin/FUNDC1/mitophagy axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Integrative Approaches to Treating Cellular Senescence in Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Hsa_circ_0101645 contributes to excessive autophagy and apoptosis in intervertebral disc degeneration by acting as a miR-1304-5p sponge modulating BNIP3 expression.Non-coding RNA research · 2026Article
- Unraveling the Mechanism of Perillyl Alcohol and Its Derivatives as Potent Antifungal Agents against Gray Mold.Journal of agricultural and food chemistry · 2026Article
- LncRNA H19 overexpression protects against acute kidney injury after cardiopulmonary bypass via activating Pink1/Parkin-mediated mitophagy.Chinese medical journal · 2026Article
- Detoxification of Ochratoxin A byFoods (Basel, Switzerland) · 2026Article
- Article
- Mitophagy and oxidative stress in chronic kidney disease (Review).Molecular medicine reports · 2026Review
31 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress is an imbalance between free radicals and the antioxidant system causing overgeneration of free radicals (oxygen-containing molecules) ultimately leading to oxidative damage in terms of lipid peroxidation, protein denaturation, and DNA mutation. Oxidative stress can activate autophagy to alleviate oxidative damage and maintain normal physiological activities of cells by degrading damaged organelles or local cytoplasm. When oxidative stress is not eliminated by autophagy, it activates the apoptosis cascade. This review provides a brief summary of mitochondrial-endoplasmic reticulum communication-mediated oxidative stress and autophagy. Mitochondria and endoplasmic reticulum being important organelles in cells are directly or indirectly connected to each other through mitochondria-associated endoplasmic reticulum membranes and jointly regulate oxidative stress and autophagy. The reactive oxygen species (ROS) produced by the mitochondrial respiratory chain are the main inducers of oxidative stress. Damaged mitochondria can be effectively cleared by the process of mitophagy mediated by PINK1/parkin pathway, Nix/BNIP3 pathways, and FUNDC1 pathway, avoiding excessive ROS production. However, the mechanism of mitochondrial-endoplasmic reticulum communication in the regulation of oxidative stress and autophagy is rarely known. For this reason, this review explores the mutual connection of mitochondria and endoplasmic reticulum in mediating oxidative stress and autophagy through ROS and Ca
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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.