ReviewRedox biology2020
An evolutionary, or "Mitocentric" perspective on cellular function and disease.
Review in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 30 citations in OpenAlex.
- Multi-tissue metabolomics reveal mtDNA- and diet-specific metabolite profiles in a mouse model of cardiometabolic disease.Redox biology · 2025Article
- Differential Mitochondrial Genome Expression of Four Skink Species Under High-Temperature Stress and Selection Pressure Analyses in Scincidae.Animals : an open access journal from MDPI · 2025Article
- Targeting the epigenome and tumor heterogeneity: advances in immunotherapy for chemoresistant metastatic colorectal cancer.Frontiers in immunology · 2025Review
- Comparison of Mitochondrial Genome Expression Differences among Four Skink Species Distributed at Different Latitudes under Low-Temperature Stress.International journal of molecular sciences · 2024Article
- The relationship and clinical significance of lactylation modification in digestive system tumors.Cancer cell international · 2024Review
- Mitochondrial Protein-Coding Gene Expression in the LizardAnimals : an open access journal from MDPI · 2024Article
- Conservation Mitonuclear Replacement: Facilitated mitochondrial adaptation for a changing world.Evolutionary applications · 2024Article
- Mitochondrial Genetics and Function as Determinants of Bone Phenotype and Aging.Current osteoporosis reports · 2023Review
- Roles of mitochondrial genetics in cancer metastasis.Trends in cancer · 2022Review
- Chronic Lung Allograft Dysfunction Is Associated with Increased Levels of Cell-Free Mitochondrial DNA in Bronchoalveolar Lavage Fluid of Lung Transplant Recipients.Journal of clinical medicine · 2022Article
- Racial Differences in XO (Xanthine Oxidase) and Mitochondrial DNA Damage-Associated Molecular Patterns in Resistant Hypertension.Hypertension (Dallas, Tex. : 1979) · 2022Article
- Targeting whole body metabolism and mitochondrial bioenergetics in the drug development for Alzheimer's disease.Acta pharmaceutica Sinica. B · 2022Review
- Decreased mitochondrial D-loop region methylation mediates an increase in mitochondrial DNA copy number in CADASIL.Clinical epigenetics · 2022Article
- Brain Energy Deficit as a Source of Oxidative Stress in Migraine: A Molecular Basis for Migraine Susceptibility.Neurochemical research · 2021Review
- Mitochondrial Metabolism in PDAC: From Better Knowledge to New Targeting Strategies.Biomedicines · 2020Review
- Blood Levels of Free-Circulating Mitochondrial DNA in Septic Shock and Postsurgical Systemic Inflammation and Its Influence on Coagulation: A Secondary Analysis of a Prospective Observational Study.Journal of clinical medicine · 2020Article
- Investigating Mitonuclear Genetic Interactions Through Machine Learning: A Case Study on Cold Adaptation Genes in Human Populations From Different European Climate Regions.Frontiers in physiology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The incidence of common, metabolic diseases (e.g. obesity, cardiovascular disease, diabetes) with complex genetic etiology has been steadily increasing nationally and globally. While identification of a genetic model that explains susceptibility and risk for these diseases has been pursued over several decades, no clear paradigm has yet been found to disentangle the genetic basis of polygenic/complex disease development. Since the evolution of the eukaryotic cell involved a symbiotic interaction between the antecedents of the mitochondrion and nucleus (which itself is a genetic hybrid), we suggest that this history provides a rational basis for investigating whether genetic interaction and co-evolution of these genomes still exists. We propose that both mitochondrial and Mendelian, or "mito-Mendelian" genetics play a significant role in cell function, and thus disease risk. This paradigm contemplates the natural variation and co-evolution of both mitochondrial and nuclear DNA backgrounds on multiple mitochondrial functions that are discussed herein, including energy production, cell signaling and immune response, which collectively can influence disease development. At the nexus of these processes is the economy of mitochondrial metabolism, programmed by both mitochondrial and nuclear genomes.
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.