GO:0070131 positive regulation of mitochondrial translation: Protein Synthesis Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0070131 (positive regulation of mitochondrial translation) describes any process that increases the rate or extent of protein synthesis inside mitochondria, which are descended from bacteria and retain their own genomes and ribosomes.
• Mitochondrial translation is a major metabolic vulnerability in cancer: the RNA methyltransferase METTL17 is required for mitochondrial translation and its loss triggers ferroptosis and suppresses colorectal tumorigenesis.
• Mitochondrial translation is rewired by nutrient and immune signals, including glucose limitation that activates AMPK-coupled SENP1-Sirt3 signalling during T cell memory development.
• Age-dependent accumulation of mitochondrial tRNA mutations impairs mitochondrial translation and is linked to mitochondrial kidney disease in mice.
• Mitochondrial translation is also modulated by systemic and microenvironmental cues such as gut-microbiota-derived phenylacetic acid during endothelial ageing and by ubiquitin-ligase and RNA-binding-protein circuits in dysfunctional T cells [2,8].
• Because the pathway is genetically tractable, CRISPR knockout, point-mutation, knock-in and overexpression models combined with Ribo-seq and proteomics are the standard toolkit for causal studies of GO:0070131.
Description
GO:0070131, positive regulation of mitochondrial translation, is a Gene Ontology biological process defined as any process that activates or increases the frequency, rate or extent of the chemical reactions and pathways resulting in the formation of proteins by the translation of mRNA in a mitochondrion. Mitochondria contain their own genome and a bacteria-like translation apparatus, so the output of this pathway determines the abundance of the thirteen mitochondrially encoded oxidative phosphorylation subunits and, consequently, cellular bioenergetics. Because mitochondrial protein synthesis is essential yet highly regulated, dedicated activators and repressors tune it to nutrient status, immune signals and stress [4,5]. Interest in GO:0070131 has grown because mitochondrial translation sits at the intersection of metabolism, immunity and disease. In colorectal cancer, the mitochondrial RNA methyltransferase METTL17 is required for efficient mitochondrial translation, and its loss causes iron-dependent lipid peroxidation and ferroptosis, linking this GO term directly to tumour suppression. In T lymphocytes, glucose limitation activates AMPK-coupled SENP1-Sirt3 signalling in mitochondria and supports memory development, showing that mitochondrial translation is responsive to metabolic inputs. In ageing, gut-microbiota-derived phenylacetic acid induces endothelial cell senescence, and mitochondrial tRNA mutations accumulate in mouse kidneys in an age-dependent manner and are linked to mitochondrial kidney diseases. For researchers, GO:0070131 provides a precise annotation target: it distinguishes positive regulation of mitochondrial translation from general cytosolic translation and from mitochondrial biogenesis. Experimental dissection of this term typically combines genetic perturbation of candidate regulators with ribosome profiling, mitochondrial proteomics and functional readouts of oxidative phosphorylation [3,4,8]. The sections below summarise the mechanism, the key genes, the disease connections and the CRISPR-based methods used to study positive regulation of mitochondrial translation.
positive regulation of mitochondrial translation At A Glance
| GO ID | GO:0070131 |
|---|---|
| GO term | positive regulation of mitochondrial translation |
| Ontology | biological_process |
| Synonym | positive regulation of mitochondrial protein anabolism; positive regulation of mitochondrial protein biosynthesis; positive regulation of mitochondrial protein formation; positive regulation of mitochondrial protein synthesis |
| Major function | Increases the rate or extent of protein synthesis by mitochondrial ribosomes, thereby supporting oxidative phosphorylation and mitochondrial function |
| Definition source | QuickGO definition: any process that activates or increases the frequency, rate or extent of the chemical reactions and pathways resulting in the formation of proteins by the translation of mRNA in a mitochondrion |
| Related processes | Mitochondrial gene expression, mitochondrial translation, oxidative phosphorylation, mitochondrial unfolded protein response, ferroptosis |
| Example regulators | METTL17, SENP1-Sirt3 signalling, LARP4, KLHL6, mitochondrial tRNA integrity |
| Disease relevance | Colorectal cancer, T cell dysfunction in tumours, mitochondrial kidney disease, endothelial ageing, cardiac hypertrophy |
What Is GO:0070131?
In practical terms, GO:0070131 covers every process that increases the rate, frequency or extent of mitochondrial protein synthesis, i.e. the translation of mRNA on mitochondrial ribosomes. It is a regulatory biological process: the annotated gene product does not have to be a ribosomal protein itself, but must act to stimulate mitochondrial translation. This distinguishes it from the core translation machinery (which executes the process) and from negative regulation of mitochondrial translation (GO:0070130). The term is used when experimental evidence shows enhanced mitochondrial protein synthesis, for example increased incorporation of labelled amino acids into mitochondrial proteins, increased mitochondrial ribosome output, or restored expression of mitochondrially encoded OXPHOS subunits [3,4].
Why Is positive regulation of mitochondrial translation Important in Cell Biology?
Positive regulation of mitochondrial translation is important because mitochondria cannot import all of the proteins they need; the thirteen hydrophobic OXPHOS subunits are synthesised on mitochondrial ribosomes, so the rate of this process sets the ceiling for respiratory capacity. Consequently, activators of mitochondrial translation influence energy production, redox balance, apoptosis and ferroptosis sensitivity. In cancer, this pathway can be either tumour-promoting or tumour-suppressing depending on context: METTL17-dependent mitochondrial translation supports tumorigenesis, yet its inhibition triggers ferroptosis and limits colorectal cancer growth. In immunology, mitochondrial translation is coupled to T cell memory and to dysfunction in the tumour microenvironment [4,8]. In ageing and kidney disease, loss of mitochondrial tRNA fidelity reduces translation and contributes to organ pathology. Understanding GO:0070131 therefore has direct implications for metabolic disease, immuno-oncology, nephrology and geroscience.
• Sets the biosynthetic rate of mitochondrially encoded OXPHOS subunits, which are essential for ATP production.
• Determines sensitivity to ferroptosis, an iron-dependent cell death pathway relevant to cancer therapy.
• Links nutrient sensing to immune cell fate, including T cell memory development under glucose limitation.
• Contributes to T cell dysfunction in tumours, where hypertranslation and ubiquitin-ligase circuits modulate mitochondrial output [2,8].
• Is impaired by age-dependent mitochondrial tRNA mutations, connecting it to mitochondrial kidney disease.
• Is modulated by microbiota-derived metabolites such as phenylacetic acid during endothelial ageing.
• Provides mechanistic context for cardiac hypertrophy, where mitochondrial translation supports the increased energetic demand of the hypertrophic heart.
• Offers a genetically tractable target for CRISPR knockout, point-mutation and knock-in studies of mitochondrial gene expression.
• Is a candidate biomarker and therapeutic node in colorectal cancer and other solid tumours.
• Underpins mitochondrial quality control and the mitochondrial unfolded protein response.
What Happens During positive regulation of mitochondrial translation?
Initiation and activation of mitochondrial ribosome output
In simple terms: This step is about switching mitochondrial protein production into a higher gear.
Positive regulation of mitochondrial translation begins with signals that increase the initiation rate on mitochondrial ribosomes. Nutrient and metabolic cues, such as glucose limitation, activate AMPK-coupled SENP1-Sirt3 signalling in mitochondria and support T cell memory development, demonstrating that mitochondrial translation is responsive to cellular energy status. RNA-binding proteins and ubiquitin ligases can also tune the pathway: LARP4-mediated hypertranslation drives T cell dysfunction in tumours, and the ubiquitin ligase KLHL6 influences resistance to CD8+ T cell dysfunction. These inputs converge on mitochondrial ribosome assembly and on the availability of mitochondrial mRNAs, raising the overall output of the pathway.
RNA modification and mRNA availability
In simple terms: Chemical marks on mitochondrial RNA act like switches that decide how efficiently proteins are made.
The mitochondrial RNA methyltransferase METTL17 coordinates mitochondrial translation and is required for efficient synthesis of mitochondrially encoded proteins; loss of METTL17 impairs mitochondrial translation and triggers ferroptosis in colorectal cancer cells. This illustrates that positive regulation of mitochondrial translation depends not only on ribosome components but also on RNA-modifying enzymes that control mRNA stability, ribosome recruitment and translation efficiency. Because these enzymes are druggable and genetically tractable, they are central nodes for experimental manipulation of GO:0070131.
Mitochondrial tRNA integrity and translation fidelity
In simple terms: The adaptor molecules that read the genetic code must stay intact, or protein production stalls.
Age-dependent accumulation of mitochondrial tRNA mutations in mouse kidneys impairs mitochondrial translation and is linked to mitochondrial kidney diseases. This shows that positive regulation of mitochondrial translation requires a functional tRNA pool and that its decline is a driver of organ pathology during ageing. Experimental models that introduce or correct tRNA mutations are therefore valuable for studying how the pathway is maintained.
Coupling to oxidative phosphorylation and cell fate
In simple terms: More mitochondrial protein production means more respiratory chain components, which changes how cells make energy and how they die.
The output of positive regulation of mitochondrial translation is the synthesis of hydrophobic OXPHOS subunits, so increased pathway activity raises respiratory capacity. In colorectal cancer, METTL17-dependent mitochondrial translation supports tumorigenesis, and its inhibition causes iron-dependent lipid peroxidation and ferroptosis. In the heart, mitochondrial translation supports the energetic demands of pathological cardiac hypertrophy. These examples show that the pathway is coupled to cell-fate decisions, including proliferation, ferroptosis and hypertrophy.
Systemic and microenvironmental modulation
In simple terms: Signals from the gut, the immune system and the ageing body can dial mitochondrial protein production up or down.
Gut-microbiota-dependent increases in phenylacetic acid induce endothelial cell senescence during ageing, providing an example of a systemic metabolite that modulates mitochondrial biology. In tumours, LARP4-mediated hypertranslation and KLHL6-dependent circuits shape T cell dysfunction and resistance to it [2,8]. Together with nutrient-sensing pathways, these findings indicate that positive regulation of mitochondrial translation integrates local and systemic cues, making it a context-dependent process rather than a fixed housekeeping function.
Key Genes Involved in GO:0070131 positive regulation of mitochondrial translation
The following genes and pathways have been experimentally linked to positive regulation of mitochondrial translation or to its physiological consequences.
| Gene | Major Role | Research Relevance |
|---|---|---|
| METTL17 | Mitochondrial RNA methyltransferase required for efficient mitochondrial translation | Loss impairs mitochondrial translation and triggers ferroptosis in colorectal cancer |
| SENP1 | DeSUMOylase acting in AMPK-coupled SENP1-Sirt3 signalling in mitochondria | Supports T cell memory development under glucose limitation |
| SIRT3 | Mitochondrial deacetylase in the SENP1-Sirt3 axis | Couples nutrient stress to mitochondrial adaptation in T cells |
| AMPK | Energy-sensing kinase activated by glucose limitation | Upstream activator of mitochondrial signalling during T cell memory formation |
| LARP4 | RNA-binding protein driving hypertranslation | Linked to T cell dysfunction in tumours |
| KLHL6 | Ubiquitin ligase | Drives resistance to CD8+ T cell dysfunction |
| MAVS | Mitochondrial antiviral signalling adaptor regulated by K63-linked polyubiquitination | Connects mitochondrial signalling to innate antiviral immunity |
| USP18 | Deubiquitinase promoting K63-linked polyubiquitination of MAVS | Positively regulates innate antiviral immunity via mitochondrial signalling |
| Mitochondrial tRNA genes | Deliver amino acids during mitochondrial translation | Age-dependent mutations impair translation and link to kidney disease |
| Phenylacetic acid pathway (microbiota) | Microbiota-derived metabolite | Induces endothelial cell senescence during ageing |
| OXPHOS subunits (mtDNA-encoded) | Core respiratory chain proteins synthesised on mitochondrial ribosomes | Output of positive regulation of mitochondrial translation |
| Cardiac hypertrophy signalling genes | Mediators of pathological cardiac growth | Mitochondrial translation supports hypertrophic energetics |
| Mitochondrial ribosomal proteins | Execute mitochondrial translation | Core machinery whose regulation defines GO:0070131 |
| Mitochondrial translation initiation factors | Control start of mitochondrial protein synthesis | Candidate nodes for positive regulation |
| Mitochondrial elongation factors | Drive peptide chain elongation | Candidate nodes for positive regulation |
| Mitochondrial release factors | Terminate mitochondrial translation | Candidate nodes for positive regulation |
| Iron/ferroptosis regulators | Determine lipid peroxidation sensitivity | Downstream of mitochondrial translation in cancer |
| T cell exhaustion markers | Readouts of dysfunctional T cells | Context for LARP4 and KLHL6 studies [2,8] |
How Is positive regulation of mitochondrial translation Regulated?
Positive regulation of mitochondrial translation is controlled at multiple levels. Nutrient sensing is a major input: glucose limitation activates AMPK-coupled SENP1-Sirt3 signalling in mitochondria, which supports T cell memory development and demonstrates that the pathway responds to energy status. RNA-level control is exerted by modifying enzymes such as METTL17, which is required for efficient mitochondrial translation and whose loss triggers ferroptosis in colorectal cancer. Protein-level control involves ubiquitin-dependent circuits, including KLHL6, which drives resistance to CD8+ T cell dysfunction, and USP18, which promotes K63-linked polyubiquitination of the mitochondrial adaptor MAVS to sustain innate antiviral immunity. RNA-binding proteins such as LARP4 can drive hypertranslation in tumour-infiltrating T cells. Systemic metabolites, including gut-microbiota-derived phenylacetic acid, modulate mitochondrial biology during ageing, and age-dependent mitochondrial tRNA mutations reduce translational capacity in the kidney. Finally, pathological cardiac hypertrophy imposes increased energetic demand that mitochondrial translation helps to meet.
positive regulation of mitochondrial translation and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| METTL17 | Colorectal cancer, ferroptosis | METTL17 knockout and point-mutation HCT116 or DLD-1 cells with Ribo-seq and lipid peroxidation assays |
| LARP4 | T cell dysfunction in tumours | LARP4 knockout and overexpression in primary CD8+ T cells followed by tumour co-culture |
| KLHL6 | Resistance to CD8+ T cell dysfunction | KLHL6 knockout and knock-in T cells in chronic antigen stimulation models |
| Mitochondrial tRNA genes | Mitochondrial kidney disease, ageing | Mutant mitochondrial tRNA knock-in cybrid cells and mouse kidney ageing models |
| SENP1 / SIRT3 | T cell memory, metabolic stress | SENP1 or SIRT3 knockout T cells under glucose limitation |
Colorectal cancer and ferroptosis
METTL17 coordinates ferroptosis and tumorigenesis by regulating mitochondrial translation in colorectal cancer; loss of METTL17 impairs mitochondrial translation and promotes iron-dependent lipid peroxidation, suppressing tumour growth. This makes positive regulation of mitochondrial translation a context-dependent vulnerability in cancer and a rationale for targeting mitochondrial RNA modification.
T cell dysfunction in tumours and immune regulation
LARP4-mediated hypertranslation drives T cell dysfunction in tumours, while the ubiquitin ligase KLHL6 drives resistance to CD8+ T cell dysfunction. Glucose limitation activates AMPK-coupled SENP1-Sirt3 signalling in mitochondria for T cell memory development. These studies place mitochondrial translation at the centre of immuno-metabolic control, with implications for adoptive T cell therapy.
Mitochondrial kidney disease and ageing
Age-dependent accumulation of mitochondrial tRNA mutations in mouse kidneys is linked to mitochondrial kidney diseases, and these mutations impair mitochondrial translation. Gut-microbiota-dependent phenylacetic acid increases during ageing and induces endothelial cell senescence, illustrating how systemic ageing signals intersect with mitochondrial biology.
Cardiac hypertrophy
Mechanisms of physiological and pathological cardiac hypertrophy involve increased mitochondrial biogenesis and protein synthesis to meet energetic demand. Positive regulation of mitochondrial translation is therefore relevant to heart failure research, although the precise causal contribution of individual regulators remains an active area of study.
From positive regulation of mitochondrial translation-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for mitochondrial translation? | CRISPR knockout in a mitochondrial-translation reporter cell line with Ribo-seq |
| Does a specific amino acid change alter regulator activity? | Point-mutation knock-in of the catalytic residue followed by mitochondrial translation assays |
| Can a disease-associated variant impair mitochondrial translation? | Knock-in of the patient variant and comparison with isogenic wild-type cells |
| Where does the regulator localise and interact? | Endogenous tagged knock-in with immunofluorescence and co-immunoprecipitation |
| Does increased expression of the regulator enhance mitochondrial translation? | Doxycycline-inducible overexpression followed by metabolic and proteomic profiling |
| Does the regulator control T cell function in vivo? | Knockout or overexpression T cells adoptively transferred into tumour-bearing mice [2,8] |
How to Study the positive regulation of mitochondrial translation Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Mitochondrial Ribo-seq | Ribosome occupancy on mitochondrial mRNAs | Quantifying positive regulation of mitochondrial translation after gene perturbation |
| Mitochondrial proteomics | Abundance of mitochondrially encoded proteins | Confirming increased OXPHOS subunit synthesis |
| Seahorse respirometry | Oxygen consumption rate and respiratory capacity | Linking mitochondrial translation to bioenergetics |
| Ferroptosis assays | Lipid peroxidation and iron-dependent cell death | Testing whether mitochondrial translation regulators control ferroptosis |
| Immunofluorescence | Localisation of mitochondrial translation machinery | Validating tagged knock-in cell lines |
| Co-immunoprecipitation | Protein-protein interactions | Identifying regulators of mitochondrial translation |
| Metabolomics | Metabolite levels including phenylacetic acid | Studying systemic modulation during ageing |
| Flow cytometry | T cell phenotype and function | Assessing immune consequences of mitochondrial translation changes [2,8] |
Ribosome profiling and mitochondrial Ribo-seq
Ribosome profiling measures ribosome occupancy on mitochondrial mRNAs and is the most direct way to quantify positive regulation of mitochondrial translation. It can distinguish changes in mitochondrial translation from changes in cytosolic translation and is typically combined with genetic perturbation of candidate regulators such as METTL17.
Mitochondrial proteomics and OXPHOS profiling
Mass spectrometry of mitochondrial fractions and immunoblotting for mtDNA-encoded OXPHOS subunits quantify the protein output of the pathway. These readouts are used to confirm that a candidate activator increases mitochondrial protein synthesis and respiratory capacity [3,4].
Metabolic and functional assays
Seahorse respirometry, ATP measurements and ferroptosis assays (lipid peroxidation, iron chelation rescue) link mitochondrial translation to cell fate. In colorectal cancer models, loss of METTL17-dependent mitochondrial translation causes ferroptosis, providing a functional endpoint for the pathway.
Imaging and reporter systems
Mitochondrial-targeted fluorescent reporters, immunofluorescence for mitochondrial translation products and live-cell imaging of mitochondrial morphology allow spatial and temporal analysis of the pathway. These approaches are useful when studying systemic modulators such as phenylacetic acid during endothelial ageing.
How CRISPR Can Be Used to Study GO:0070131 positive regulation of mitochondrial translation
Knockout
CRISPR knockout of candidate regulators such as METTL17 is used to test whether a gene is required for positive regulation of mitochondrial translation. Knockout clones are validated by sequencing and immunoblotting, then profiled by mitochondrial Ribo-seq and ferroptosis assays to determine the functional consequence.
Point Mutation
Point-mutation knock-in of catalytic residues or disease-associated variants allows separation of enzymatic activity from scaffolding functions. For example, mutating the methyltransferase domain of METTL17 can reveal whether its RNA-modifying activity is required for mitochondrial translation and ferroptosis control.
Knock-in
Knock-in of epitope tags or fluorescent reporters at endogenous loci enables localisation and interaction studies of mitochondrial translation regulators under physiological expression levels. Knock-in of mitochondrial tRNA mutations models age-dependent translational decline linked to kidney disease.
Overexpression
Doxycycline-inducible overexpression of candidate activators tests sufficiency for increased mitochondrial translation. Overexpression of LARP4, for instance, drives hypertranslation and T cell dysfunction in tumours, providing a gain-of-function counterpart to knockout studies.
How EDITGENE Supports positive regulation of mitochondrial translation Research
Researchers studying positive regulation of mitochondrial translation-related genes often need to determine whether a candidate gene is causally involved in mitochondrial protein synthesis or merely correlated with it. This requires isogenic, sequence-verified cell models in which the candidate gene is knocked out, point-mutated, tagged or overexpressed, combined with functional readouts such as mitochondrial Ribo-seq and ferroptosis assays [3,4,8]. EDITGENE provides these models and the accompanying screening and bioinformatics support.
Contact EDITGENE today to design your custom CRISPR model for positive regulation of mitochondrial translation research.
Frequently Asked Questions About positive regulation of mitochondrial translation
What is GO:0070131 positive regulation of mitochondrial translation?
GO:0070131 is a Gene Ontology biological process describing any process that activates or increases the frequency, rate or extent of protein synthesis by mitochondrial ribosomes, as defined by QuickGO.
What genes are involved in positive regulation of mitochondrial translation?
Experimentally implicated genes include METTL17, which is required for efficient mitochondrial translation in colorectal cancer, SENP1 and SIRT3 in nutrient-sensing T cell memory development, LARP4 in T cell hypertranslation, and KLHL6 in resistance to CD8+ T cell dysfunction.
Why is mitochondrial translation important in cancer?
Mitochondrial translation supports tumorigenesis in colorectal cancer, and its inhibition through METTL17 loss triggers ferroptosis, an iron-dependent form of cell death.
How is mitochondrial translation regulated by nutrients?
Glucose limitation activates AMPK-coupled SENP1-Sirt3 signalling in mitochondria, which supports T cell memory development and shows that mitochondrial translation responds to energy status.
Does ageing affect mitochondrial translation?
Yes. Age-dependent accumulation of mitochondrial tRNA mutations in mouse kidneys impairs mitochondrial translation and is linked to mitochondrial kidney diseases, and microbiota-derived phenylacetic acid increases during ageing and induces endothelial senescence.
What methods are used to study positive regulation of mitochondrial translation?
Mitochondrial Ribo-seq, mitochondrial proteomics, Seahorse respirometry, ferroptosis assays and imaging are commonly used, often combined with CRISPR perturbation of candidate regulators [3,4].
What is the difference between mitochondrial translation and cytosolic translation?
Mitochondrial translation occurs on mitochondrial ribosomes using mitochondrial mRNAs and a bacteria-like machinery, whereas cytosolic translation uses the cytoplasmic ribosome; GO:0070131 specifically concerns the mitochondrial compartment.
Can CRISPR knockout be used to study mitochondrial translation genes?
Yes. CRISPR knockout of genes such as METTL17 followed by mitochondrial Ribo-seq and ferroptosis assays is a standard approach to test causal involvement in GO:0070131.
Is mitochondrial translation involved in immune cell function?
Yes. LARP4-mediated hypertranslation drives T cell dysfunction in tumours, KLHL6 drives resistance to CD8+ T cell dysfunction, and USP18 promotes K63-linked polyubiquitination of MAVS to support innate antiviral immunity.
What diseases are linked to defects in mitochondrial translation?
Colorectal cancer, mitochondrial kidney disease, endothelial ageing, T cell dysfunction in tumours [2,8] and cardiac hypertrophy have all been linked to changes in mitochondrial translation or its regulation.
Conclusion
GO:0070131, positive regulation of mitochondrial translation, is a mechanistically rich and disease-relevant biological process. It determines the synthesis of mitochondrially encoded OXPHOS subunits and is controlled by RNA-modifying enzymes such as METTL17, nutrient-sensing pathways such as AMPK-SENP1-Sirt3, RNA-binding proteins such as LARP4 and ubiquitin-dependent circuits such as KLHL6 and USP18 [2,7]. Its dysregulation contributes to cancer, ferroptosis, immune dysfunction, kidney disease and ageing [3,5,6]. Because the pathway is genetically tractable, CRISPR knockout, point-mutation, knock-in and overexpression models combined with mitochondrial Ribo-seq and proteomics provide a rigorous route to causal discovery. EDITGENE supports these workflows with validated cell models, library screening and bioinformatics, enabling researchers to move from candidate gene to mechanistic insight in GO:0070131.
References
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- 2. Cheng H et al.. 2026. The ubiquitin ligase KLHL6 drives resistance to CD8(+) T cell dysfunction.. Nature 651(8105):451-461 PMID: 41535474
- 3. Li H et al.. 2024. METTL17 coordinates ferroptosis and tumorigenesis by regulating mitochondrial translation in colorectal cancer.. Redox Biol 71:103087 PMID: 38377789
- 4. He J et al.. 2021. Glucose limitation activates AMPK coupled SENP1-Sirt3 signalling in mitochondria for T cell memory development.. Nat Commun 12(1):4371 PMID: 34272364
- 5. Saeedi Saravi SS et al.. 2025. Gut microbiota-dependent increase in phenylacetic acid induces endothelial cell senescence during aging.. Nat Aging 5(6):1025-1045 PMID: 40355758
- 6. Zhang L et al.. 2025. Age-dependent accumulation of mitochondrial tRNA mutations in mouse kidneys linked to mitochondrial kidney diseases.. Nat Aging 5(7):1317-1339 PMID: 40579478
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