ReviewArchives of toxicology2015
Mitochondrial functional impairment in response to environmental toxins in the cardiorenal metabolic syndrome.
Review in Archives of toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 46 citations in OpenAlex.
- Molecular mechanisms of folliculogenesis and oogenesis.Systems biology in reproductive medicine · 2026Review
- The Oxidative Stress and Inflammatory Metabolic Pathways of Some Environmental Toxicants Inflicting Human Disorders.Toxics · 2026Review
- Biocompatibility and Cell Death Mechanisms Induced by PMMA-Based Dental Materials in Gingival Fibroblasts and OECM-1 Tumor Cells.Dentistry journal · 2026Article
- Article
- Mitochondria-Mediated Mechanisms of Ferroptosis in Neurological Diseases.Neurochemical research · 2025Review
- Associations of Prenatal Mercury Exposure and PUFA with Telomere Length and mtDNA Copy Number in 7-Year-Old Children in the Seychelles Child Development Nutrition Cohort 2.Environmental health perspectives · 2025Article
- Environmental Diagnosis through a Flow Cytometric Approach.International journal of molecular sciences · 2024Review
- The mediation effect of Systemic Immunity Inflammation Index between urinary metals and TOFAT among adults in the NHANES dataset.Scientific reports · 2024Article
- Metabolomics: a promising tool for deciphering metabolic impairment in heavy metal toxicities.Frontiers in molecular biosciences · 2023Review
- Environmental Chemical Exposures and Mitochondrial Dysfunction: a Review of Recent Literature.Current environmental health reports · 2022Review
- Key Characteristics of Cardiovascular Toxicants.Environmental health perspectives · 2021Article
- Epigallocatechin Gallate for Management of Heavy Metal-Induced Oxidative Stress: Mechanisms of Action, Efficacy, and Concerns.International journal of molecular sciences · 2021Review
- Article
- On the central role of mitochondria dysfunction and oxidative stress in Alzheimer's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019Review
- Mitochondrial Morphofunction in Mammalian Cells.Antioxidants & redox signaling · 2019Review
- Associations of blood mercury and fatty acid concentrations with blood mitochondrial DNA copy number in the Seychelles Child Development Nutrition Study.Environment international · 2019Article
- Mitochondrial PKC-ε deficiency promotes I/R-mediated myocardial injury via GSK3β-dependent mitochondrial permeability transition pore opening.Journal of cellular and molecular medicine · 2017Article
- Pinocembrin Attenuates Mitochondrial Dysfunction in Human Neuroblastoma SH-SY5Y Cells Exposed to Methylglyoxal: Role for the Erk1/2-Nrf2 Signaling Pathway.Neurochemical research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Environmental toxins can promote cardiovascular, metabolic, and renal abnormalities, which characterize the cardiorenal metabolic syndrome (CRS). Heavy metals, such as mercury and arsenic, represent two of the most toxic pollutants. Exposure to these toxins is increasing due to increased industrialization throughout much of the world. Studies conducted to understand the impact of environmental toxins have shown a major impact on mitochondrial structure and function. The maladaptive stress products caused by these toxins, including aggregated proteins, damaged organelles, and intracellular pathogens, can be removed through autophagy, which is also known as mitophagy in mitochondria. Although the underlying mechanisms involved in the regulation of mitophagy in response to pollution are not well understood, accumulating evidence supports a role for maladaptive mitochondrial responses to environmental pollution in the pathogenesis of the CRS. In this review, we discuss the ongoing research, which explores the mechanisms by which these toxins promote abnormalities in mitophagy and associated mitochondrial dysfunction and the CRS.
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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.