ArticleCell reports2021
Stress granules inhibit fatty acid oxidation by modulating mitochondrial permeability.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 71 citations in OpenAlex.
- Review
- Stress granule phase separation in stress-responsive cytosolic extract-in-oil droplets.Nature communications · 2026Article
- The Role of Stress Granules in Cardiovascular Diseases.Reviews in cardiovascular medicine · 2026Review
- Hepatocyte TIA1 constrains metabolic steatohepatitis by translationally suppressing Srebf1 mRNA in stress granules.Cell death & disease · 2026Article
- Androgen receptor localisation and protein interactions provide insight into steroid mediated metabolic shifts in endocrine resistant breast cancer.NPJ breast cancer · 2026Article
- Machine Learning-Assisted Quantification of Organelle Abundance.Bio-protocol · 2026Article
- Mitochondrial remodeling and metabolic reprogramming drive long-term salinity adaptation inmSystems · 2026Article
- Stress granules as a central hub linking organelle stress, aging, and neurodegeneration.BMB reports · 2026Review
- Chronic stress disrupts the network among stress granules, P-bodies, and motor proteins.bioRxiv : the preprint server for biology · 2026Article
- Differential regulation of p62-ubiquitin conjugates in neurons versus astrocytes during cellular stress.PloS one · 2026Article
- TDP-43 proteinopathies and neurodegeneration: insights from Caenorhabditis elegans models.The FEBS journal · 2026Review
- Distinct CSF lipidomic profiles are associated with five proteomic subtypes in patients with Alzheimer's disease.Molecular neurodegeneration advances · 2026Article
- Stress granule dynamics govern TOR reactivation and growth recovery during post-heat stress adaptation.Science advances · 2025Article
- The role of fatty acids in neurodegenerative diseases: mechanistic insights and therapeutic strategies.Journal of lipid research · 2025Review
- Stress granules promote quiescence by enhancing p21 levels and reducing phospho-Rb.RNA (New York, N.Y.) · 2025Article
- Protein Kinase C promotes peroxisome biogenesis and peroxisome-endoplasmic reticulum interaction.The Journal of cell biology · 2025Article
- UBAP2L-driven stress granule formation links oxaliplatin resistance to gastric cancer.Communications biology · 2025Article
- PABPC1 SUMOylation enhances cell survival by promoting mitophagy through stabilizing U-rich mRNAs within stress granules.Nature communications · 2025Article
- DEAD-Box Helicase 3 Modulates the Non-Coding RNA Pool in Ribonucleoprotein Condensates During Stress Granule Formation.Non-coding RNA · 2025Article
- NaLRR-RK4 mediates MAPK signaling to enhance plant defense against Alternaria alternata in Nicotiana attenuata.Scientific reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The formation of stress granules (SGs) is an essential aspect of the cellular response to many kinds of stress, but its adaptive role is far from clear. SG dysfunction is implicated in aging-onset neurodegenerative diseases, prompting interest in their physiological function. Here, we report that during starvation stress, SGs interact with mitochondria and regulate metabolic remodeling. We show that SG formation leads to a downregulation of fatty acid β-oxidation (FAO) through the modulation of mitochondrial voltage-dependent anion channels (VDACs), which import fatty acids (FAs) into mitochondria. The subsequent decrease in FAO during long-term starvation reduces oxidative damage and rations FAs for longer use. Failure to form SGs, whether caused by the genetic deletion of SG components or an amyotrophic lateral sclerosis (ALS)-associated mutation, translates into an inability to downregulate FAO. Because metabolic dysfunction is a common pathological element of neurodegenerative diseases, including ALS, our findings provide a direction for studying the clinical relevance of SGs.
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.