ReviewProteomics2020
Mitochondrial Dysfunction in Age-Related Metabolic Disorders.
Review in Proteomics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 77 citations in OpenAlex.
- Mitophagy and Noncoding RNA Regulation in Type 2 Diabetes Mellitus: Molecular Mechanisms, Tissue-Specific Evidence and Translational Perspective.Biomedicines · 2026Review
- Identification of Potential Biomarkers Associated with Impaired Fatty Acid Oxidation in Aged Skeletal Muscle Using Bioinformatics and Machine Learning Approaches.Biomolecules · 2026Article
- miR-214-3p exacerbates mitochondrial dysfunction in parkinson's disease: a multi-omics and mechanistic study.Experimental brain research · 2026Article
- Protective Effects of Ginsenosides on Drug-induced Cardiotoxicity: A New Therapeutic Approach with Focus on Molecular Mechanisms in Cardio-oncology Field.Current medicinal chemistry · 2026Review
- Cleaning, Chasing and Calming: Promising Paradigms of Senotherapy in Aging-Related Diseases.International journal of biological sciences · 2026Review
- Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Plin2 Coordinates Immune and Metabolic Reprogramming in Lacrimal Gland Aging.Investigative ophthalmology & visual science · 2025Article
- Longevity mechanisms in cardiac aging: exploring calcium dysregulation and senescence.Biogerontology · 2025Review
- Pinitol Improves Lipopolysaccharide-Induced Cellular Damage in Human Dermal Microvascular Endothelial Cells.Molecules (Basel, Switzerland) · 2025Article
- Comparative Transcriptomic Analysis Reveals New Insights into Spawn Aging inInternational journal of molecular sciences · 2025Article
- Female reproductive capacity preservation: antioxidant strategies in combating ovarian aging and cryopreservation challenges.Frontiers in endocrinology · 2025Review
- Article
- PINK1/Parkin-Mediated Mitophagy Ameliorates Mitochondrial Dysfunction in Lacrimal Gland Acinar Cells During Aging.Investigative ophthalmology & visual science · 2024Article
- Associations of Amino Acids with the Risk of Prediabetes: A Case-Control Study from Kazakhstan.Journal of personalized medicine · 2024Article
- Ferulic acid restores mitochondrial dynamics and autophagy via AMPK signaling pathway in a palmitate-induced hepatocyte model of metabolic syndrome.Scientific reports · 2024Article
- Hair Growth Promoting Effects of 15-Hydroxyprostaglandin Dehydrogenase Inhibitor in Human Follicle Dermal Papilla Cells.International journal of molecular sciences · 2024Article
- Engineered Mitochondrial Transplantation as An Anti-Aging Therapy.Aging and disease · 2024Review
- Proline restores mitochondrial function and reverses aging hallmarks in senescent cells.Cell reports · 2024Article
- Contributing roles of mitochondrial dysfunction and hepatocyte apoptosis in liver diseases through oxidative stress, post-translational modifications, inflammation, and intestinal barrier dysfunction.Cellular and molecular life sciences : CMLS · 2024Review
- Aging mitochondria in the context of SARS-CoV-2: exploring interactions and implications.Frontiers in aging · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Aging is a natural biological process in living organisms characterized by receding bioenergetics. Mitochondria are crucial for cellular bioenergetics and thus an important contributor to age-related energetics deterioration. In addition, mitochondria play a major role in calcium signaling, redox homeostasis, and thermogenesis making this organelle a major cellular component that dictates the fate of a cell. To maintain its quantity and quality, mitochondria undergo multiple processes such as fission, fusion, and mitophagy to eliminate or replace damaged mitochondria. While this bioenergetics machinery is properly protected, the functional decline associated with age and age-related metabolic diseases is mostly a result of failure in such protective mechanisms. In addition, metabolic by-products like reactive oxygen species also aid in this destructive pathway. Mitochondrial dysfunction has always been thought to be associated with diseases. Moreover, studies in recent years have pointed out that aging contributes to the decay of mitochondrial health by promoting imbalances in key mitochondrial-regulated pathways. Hence, it is crucial to understand the nexus of mitochondrial dysfunction in age-related diseases. This review focuses on various aspects of basic mitochondrial biology and its status in aging and age-related metabolic diseases.
Indexed as
Identifiers
What Socratic 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 Socratic graph.