ArticleCell research2018
Switching off IMMP2L signaling drives senescence via simultaneous metabolic alteration and blockage of cell death.
Article in Cell research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 54 citations in OpenAlex.
- Grape Seed Proanthocyanidin Extract (GSPE) Mitigates Preterm White Matter Injury in Mice Via Improving Mitochondrial Homeostasis and Activity of IMMP2L-Related Signaling Pathway.Neurochemical research · 2026Article
- YAP1 Dysfunction Promotes Molecular Properties Linked to Breast Cancer Susceptibility.Cancer prevention research (Philadelphia, Pa.) · 2026Article
- Determination of ADP/ATP translocase isoform ratios in malignancy and cellular senescence.Molecular oncology · 2025Article
- Inner Mitochondrial Membrane Peptidase 2-Like Deletion Aggravates Mitochondrial Apoptosis and Inhibits Autophagy After Hyperglycemia Stroke.Molecular neurobiology · 2025Article
- Cellular senescence in age-related musculoskeletal diseases.Frontiers of medicine · 2025Review
- A transcriptome-based human universal senescence index (hUSI) robustly predicts cellular senescence under various conditions.Nature aging · 2025Article
- Transcriptional Heterogeneity and Differential Response of Rod Photoreceptor Pathway Uncovered by Single-Cell RNA Sequencing of the Aging Mouse Retina.Aging cell · 2025Article
- Article
- Glycerol 3-phosphate dehydrogenases (1 and 2) in cancer and other diseases.Experimental & molecular medicine · 2024Review
- Immp2l Enhances the Structure and Function of Mitochondrial Gpd2 Dehydrogenase.International journal of molecular sciences · 2024Article
- Branched-Chain Amino Acid Accumulation Fuels the Senescence-Associated Secretory Phenotype.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- An advanced comprehensive muti-cell-type-specific model for predicting anti-PD-1 therapeutic effect in melanoma.Theranostics · 2024Article
- Review
- Antagonizing the irreversible thrombomodulin-initiated proteolytic signaling alleviates age-related liver fibrosis via senescent cell killing.Cell research · 2023Article
- Review
- SERPINB4 Promotes Keratinocyte Inflammation via p38MAPK Signaling Pathway.Journal of immunology research · 2023Article
- Establishing a human bone marrow single cell reference atlas to study ageing and diseases.Frontiers in immunology · 2023Article
- Genetic signature of differentiated thyroid carcinoma susceptibility: a machine learning approach.European thyroid journal · 2022Article
- Contribution of proteases to the hallmarks of aging and to age-related neurodegeneration.Aging cell · 2022Review
- Squamous Cell Carcinoma Antigen: Clinical Application and Research Status.Diagnostics (Basel, Switzerland) · 2022Review
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
Cellular senescence is a fundamental cell fate playing a significant role throughout the natural aging process. However, the molecular determinants distinguishing senescence from other cell-cycle arrest states such as quiescence and post-mitotic state, and the specified mechanisms underlying cell-fate decisions towards senescence versus cell death in response to cellular stress stimuli remain less understood. Employing multi-omics approaches, we revealed that switching off the specific mitochondrial processing machinery involving the peptidase IMMP2L serves as the foundation of the senescence program, which was also observed during the mammalian aging process. Mechanistically, we demonstrate that IMMP2L processes and thus activates at least two substrates, mitochondrial metabolic enzyme glycerol-3-phosphate dehydrogenase (GPD2) and cell death regulator apoptosis-inducing factor (AIF). For cells destined to senesce, concerted shutdown of the IMMP2L-GPD2 and IMMP2L-AIF signaling axes collaboratively drives the senescent process by reprogramming mitochondria-associated redox status, phospholipid metabolism and signaling network, and simultaneously blocking cell death under oxidative stress conditions.
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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.