ReviewAntioxidants (Basel, Switzerland)2025
MAPK Signaling in the Interplay Between Oxidative Stress and Autophagy.
Review in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Investigating the clinical efficacy, safety and molecular mechanism of sulforaphane in autism spectrum disorder: an integrated study combining meta-analysis, network pharmacology, and computational biology.BMC pharmacology & toxicology · 2025Pooled it
- FOXM1 downregulation contributes to sevoflurane-induced microglial dysfunction via transcriptional downregulation of RGS10.Experimental brain research · 2026Article
- Small-molecule autophagy modulators: Mechanisms, therapeutic potential, and development challenges in pathological settings.Fundamental research · 2026Review
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Liposomal Piceatannol Mitigates Methotrexate-Induced Oxidative Renal Injury via Modulation of Nrf2/HO-1, TLR4/NF-κB, MAPK, and Apoptotic Pathways in Rats.Biomolecules · 2026Article
- Nutritional Strategies and Aging: Current Evidence and Future Directions.Molecules (Basel, Switzerland) · 2026Review
- TM9SF1 Aggravates Liver Ischemia-Reperfusion Injury by Promoting Autophagy.Inflammation · 2026Article
- From Phytochemistry to Oncology: The Role of Bakuchiol in the Treatment of Breast Cancer.Biomolecules · 2026Review
- Molecular mechanisms of autophagy-lysosomal pathway dysfunction in neurodegenerative diseases and therapeutic strategies for lysosomal repair: a review.Frontiers in neuroscience · 2026Review
- Apoptosis as an evolutionary battleground: pathogen pressure and the shaping of programmed cell death pathways.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The term autophagy identifies several mechanisms that mediate the degradation of intracellular and extracellular components via the lysosomal pathway. Three main forms of autophagy exist, namely macroautophagy, chaperone-mediated autophagy, and endosomal microautophagy, which have distinct mechanisms but share lysosomes as the final destination of their cargo. A basal autophagic flux is crucial for the maintenance of cellular homeostasis, being involved in the physiological turnover of proteins and organelles. Several stressors, including nutrient shortage and genotoxic and oxidative stress, increase the autophagic rate, which prevents the accumulation of damaged and potentially harmful cell components, thus preserving cell viability. In this context, several studies have highlighted the role of MAPKs, serine-threonine kinases activated by several stimuli, in linking oxidative stress and autophagy. Indeed, several oxidative stressors activate autophagy by converging on MAPKs, directly or indirectly. In this regard, the different transcription factors that bridge MAPKs and autophagic activation are here described. In this review, we summarize the current knowledge regarding the regulation of autophagy by MAPK, including the atypical ones, with a particular focus on the regulation of autophagy by oxidative stress.
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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 Socratic graph.