ReviewGenes2018
The Aging Mitochondria.
Review in Genes, 2018. 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, 97 citations in OpenAlex.
- Ginger Bioactives as Multi-Target Therapeutics: Mechanisms, Delivery Innovation, and Human Health Impact.Nutrients · 2026Review
- The cellular choreography of brain aging: a neuroimmune network perspective.Frontiers in aging neuroscience · 2026Review
- Inter-Caste Comparison Reveals a Unique Bioenergetic Signature in Long-Lived Ant Queens.Molecular ecology · 2025Article
- HMGB1 and mitochondrial dysfunction: a double-edged sword in ageing.Open biology · 2025Review
- Review
- Unravelling the Connection Between Energy Metabolism and Immune Senescence/Exhaustion in Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.Biomolecules · 2025Review
- Reactive oxygen species: balancing agents in plants.Frontiers in plant science · 2025Review
- Multi-omics analysis reveals the genetic aging landscape of Parkinson's disease.Scientific reports · 2024Article
- Harnessing Artificial Intelligence for the Detection and Management of Colorectal Cancer Treatment.Cancer prevention research (Philadelphia, Pa.) · 2024Review
- Effects of Ginger (Biomolecules · 2024Review
- Role of umbilical cord mesenchymal stromal cells in skin rejuvenation.NPJ Regenerative medicine · 2024Review
- Cardiovascular aging: spotlight on mitochondria.American journal of physiology. Heart and circulatory physiology · 2024Review
- Talk to Me-Interplay between Mitochondria and Microbiota in Aging.International journal of molecular sciences · 2023Review
- Young Astrocytic Mitochondria Attenuate the Elevated Level of CCL11 in the Aged Mice, Contributing to Cognitive Function Improvement.International journal of molecular sciences · 2023Article
- Klotho, Oxidative Stress, and Mitochondrial Damage in Kidney Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Biological aging processes underlying cognitive decline and neurodegenerative disease.The Journal of clinical investigation · 2022Review
- Role of angiotensin II in aging.Frontiers in aging neuroscience · 2022Review
- Regulation of mitochondrial cargo-selective autophagy by posttranslational modifications.The Journal of biological chemistry · 2021Review
- Mitochondrial links between brain aging and Alzheimer's disease.Translational neurodegeneration · 2021Review
- The Chemistry of Reactive Oxygen Species (ROS) Revisited: Outlining Their Role in Biological Macromolecules (DNA, Lipids and Proteins) and Induced Pathologies.International journal of molecular sciences · 2021Review
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
Mitochondrial dysfunction is a central event in many pathologies and contributes as well to age-related processes. However, distinguishing between primary mitochondrial dysfunction driving aging and a secondary mitochondrial impairment resulting from other cell alterations remains challenging. Indeed, even though mitochondria undeniably play a crucial role in aging pathways at the cellular and organismal level, the original hypothesis in which mitochondrial dysfunction and production of free radicals represent the main driving force of cell degeneration has been strongly challenged. In this review, we will first describe mitochondrial dysfunctions observed in aged tissue, and how these features have been linked to mitochondrial reactive oxygen species (ROS)-mediated cell damage and mitochondrial DNA (mtDNA) mutations. We will also discuss the clues that led to consider mitochondria as the starting point in the aging process, and how recent research has showed that the mitochondria aging axis represents instead a more complex and multifactorial signaling pathway. New working hypothesis will be also presented in which mitochondria are considered at the center of a complex web of cell dysfunctions that eventually leads to cell senescence and death.
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.