ArticleNature communications2022
Mitochondrial protein import determines lifespan through metabolic reprogramming and de novo serine biosynthesis.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 51 citations in OpenAlex.
- Metabolic Profiling of Epigenetic Aging and Its Associations With Aging-Related Phenotypes and Modifiable Lifestyle Factors.Aging cell · 2026Article
- The hallmarks of protein and amino acid restriction in aging and longevity.Cell press blue · 2026Article
- Mitochondrial stress activates ELT-2-dependent lysosomal proteostasis to extend lifespan inScience advances · 2026Article
- Transcriptomic analysis of mitohormesis associated with lifespan extension in Caenorhabditis elegans.GeroScience · 2026Article
- Serine Hydroxymethyltransferase (SHMT) in biology and disease: molecular mechanisms and therapeutic targeting.Journal of translational medicine · 2026Review
- Adaptive ER stress promotes mitochondrial remodelling and longevity through PERK-dependent MERCS assembly.Cell death and differentiation · 2026Article
- An Alternative Metabolic Pathway of Glucose Oxidation Induced by Mitochondrial Complex I Inhibition: Serinogenesis and Folate Cycling.International journal of molecular sciences · 2025Article
- Leucine inhibits degradation of outer mitochondrial membrane proteins to adapt mitochondrial respiration.Nature cell biology · 2025Article
- Phase separation meets energy generation to boost longevity.Nature aging · 2025Article
- The role of pyruvate dehydrogenase in the lifespan determination of daphnids.Nature communications · 2025Article
- Serine metabolism in aging and age-related diseases.GeroScience · 2025Review
- Mitochondrial protein import stress.Nature cell biology · 2025Review
- Metformin modulates the unfolded protein responses, altering lifespan and health-promoting effects in UPR-activated worms.PloS one · 2025Article
- A Brief Review on Caenorhabditis elegans Role in Modelling Neurodegenerative Disease.Central nervous system agents in medicinal chemistry · 2025Review
- Preventing excessive autophagy protects from the pathology of mtDNA mutations in Drosophila melanogaster.Nature communications · 2024Article
- The Quest for Eternal Youth: Hallmarks of Aging and Rejuvenating Therapeutic Strategies.Biomedicines · 2024Review
- Review
- Spermidine is essential for fasting-mediated autophagy and longevity.Nature cell biology · 2024Article
- Study on the inhibitory activity and mechanism of Mentha haplocalyx essential oil nanoemulsion against Fusarium oxysporum growth.Scientific reports · 2024Article
- Metabolic mechanisms of species-specific developmental tempo.Developmental cell · 2024Review
Corrections and comments
- Commented on by
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sustained mitochondrial fitness relies on coordinated biogenesis and clearance. Both processes are regulated by constant targeting of proteins into the organelle. Thus, mitochondrial protein import sets the pace for mitochondrial abundance and function. However, our understanding of mitochondrial protein translocation as a regulator of longevity remains enigmatic. Here, we targeted the main protein import translocases and assessed their contribution to mitochondrial abundance and organismal physiology. We find that reduction in cellular mitochondrial load through mitochondrial protein import system suppression, referred to as MitoMISS, elicits a distinct longevity paradigm. We show that MitoMISS triggers the mitochondrial unfolded protein response, orchestrating an adaptive reprogramming of metabolism. Glycolysis and de novo serine biosynthesis are causatively linked to longevity, whilst mitochondrial chaperone induction is dispensable for lifespan extension. Our findings extent the pro-longevity role of UPR
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.