ReviewThe FEBS journal2021
Targeting cellular senescence based on interorganelle communication, multilevel proteostasis, and metabolic control.
Review in The FEBS journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 35 citations in OpenAlex.
- Alpha-Ketoglutarate Attenuates UVB-Induced Skin Photoaging by Restoring Mitochondrial Redox Homeostasis.Antioxidants (Basel, Switzerland) · 2026Article
- Intercompartmental communication in senescence.FEBS open bio · 2026Review
- Mitochondria-endoplasmic reticulum contact sites in hepatocytic senescence.Cellular & molecular biology letters · 2026Review
- Comprehensive profiling of circRNAs reveals stimulus-specific networks and core regulators of cellular senescence.PloS one · 2026Article
- Synergistic interplay between UV and urban particulate matter exposure induces melanocyte senescence and contributes to human skin aging.Scientific reports · 2025Article
- Urolithin Α modulates inter-organellar communication via calcium-dependent mitophagy to promote healthy ageing.Autophagy · 2025Article
- Enhancing Late-Life Survival and Mobility via Mitohormesis by Reducing Mitochondrial Calcium Levels.Aging cell · 2025Article
- Role of Mitochondrial Dynamics in Skin Homeostasis: An Update.International journal of molecular sciences · 2025Review
- Correlation of organelle interactions in the development of non-alcoholic fatty liver disease.Frontiers in immunology · 2025Review
- Overview of distinct 8-oxoguanine profiles of messenger RNA in normal and senescent cancer cells.Frontiers in cell and developmental biology · 2025Article
- Review
- Redox regulation of UPR signalling and mitochondrial ER contact sites.Cellular and molecular life sciences : CMLS · 2024Review
- Article
- 2'-O-ribose methylation levels of ribosomal RNA distinguish different types of growth arrest in human dermal fibroblasts.Journal of cell science · 2024Article
- C-X-C chemokine receptor type 4 promotes tubular cell senescence and renal fibrosis through β-catenin-inhibited fatty acid oxidation.Journal of cellular and molecular medicine · 2024Article
- HKDC1, a target of TFEB, is essential to maintain both mitochondrial and lysosomal homeostasis, preventing cellular senescence.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Oxidative Stress-Induced Cellular Senescence: Is Labile Iron the Connecting Link?Antioxidants (Basel, Switzerland) · 2023Review
- Mitochondrial dynamics and metabolism across skin cells: implications for skin homeostasis and aging.Frontiers in physiology · 2023Review
- Cinnamaldehyde attenuates kidney senescence and injury through PI3K/Akt pathway-mediated autophagy via downregulating miR-155.Renal failure · 2022Article
- Targeting senescent cells for a healthier longevity: the roadmap for an era of global aging.Life medicine · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Cellular senescence, a stable cell division arrest caused by severe damage and stress, is a hallmark of aging in vertebrates including humans. With progressing age, senescent cells accumulate in a variety of mammalian tissues, where they contribute to tissue aging, identifying cellular senescence as a major target to delay or prevent aging. There is an increasing demand for the discovery of new classes of small molecules that would either avoid or postpone cellular senescence by selectively eliminating senescent cells from the body (i.e., 'senolytics') or inactivating/switching damage-inducing properties of senescent cells (i.e., 'senostatics/senomorphics'), such as the senescence-associated secretory phenotype. Whereas compounds with senolytic or senostatic activity have already been described, their efficacy and specificity has not been fully established for clinical use yet. Here, we review mechanisms of senescence that are related to mitochondria and their interorganelle communication, and the involvement of proteostasis networks and metabolic control in the senescent phenotype. These cellular functions are associated with cellular senescence in in vitro and in vivo models but have not been fully exploited for the search of new compounds to counteract senescence yet. Therefore, we explore possibilities to target these mechanisms as new opportunities to selectively eliminate and/or disable senescent cells with the aim of tissue rejuvenation. We assume that this research will provide new compounds from the chemical space which act as mimetics of caloric restriction, modulators of calcium signaling and mitochondrial physiology, or as proteostasis optimizers, bearing the potential to counteract cellular senescence, thereby allowing healthy aging.
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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.