ReviewJournal of diabetes investigation2013
Extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine-disrupting chemicals and biophysical laws.
Review in Journal of diabetes investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Association between polychlorinated biphenyl (PCB) and dioxin with metabolic syndrome (METS): a systematic review and meta-analysis.Scientific reports · 2024Pooled it
- Implications of Endocrine-Disrupting Chemicals for Human Health and Effective Methods for Prevention and Reduction.Toxics · 2026Review
- The role of SIRT2 in vascular-related and heart-related diseases: A review.Journal of cellular and molecular medicine · 2021Review
- Childhood obesity and endocrine disrupting chemicals.Annals of pediatric endocrinology & metabolism · 2017Review
- Metformin as an anticancer drug: A Commentary on the metabolic determinants of cancer cell sensitivity to glucose limitation and biguanides.Journal of diabetes investigation · 2015Article
- Metabolic syndrome and the environmental pollutants from mitochondrial perspectives.Reviews in endocrine & metabolic disorders · 2014Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic syndrome and its component phenotypes, hyperglycemia, hypertension, (abdominal) obesity and hypertriglyceridemia, are major risk factors for atherosclerosis. Recently, associations between exposure to endocrine-disrupting chemicals (EDCs), mitochondrial dysfunction, metabolic syndrome and atherosclerosis have been established, suggesting a possible common mechanism underlying these phenomena. Extending a previously proposed mitochondria dysfunction theory of metabolic syndrome and using biophysical laws, such as metabolic scaling, Murray's law and fractal geometry of the vascular branching system, we propose that atherosclerosis could be explained as an ill-adaptive change occurring in nutrient-supplying arteries in response to the decreasing tissue energy demand caused by tissue mitochondrial dysfunction. Various aspects of this new hypothesis are discussed.
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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.