ReviewNutrients2024
4-Hydroxynonenal from Mitochondrial and Dietary Sources Causes Lysosomal Cell Death for Lifestyle-Related Diseases.
Review in Nutrients, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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Who cites it
16 citing papers in PubMed.
- Membrane-Targeted Consequences of Acetaminophen Toxicity and Off-Target Effects of Antimicrobial Peptides on Host Cell Membranes.International journal of molecular sciences · 2026Review
- Aldh3a1-mediated detoxification of reactive aldehydes contributes to distinct muscle responses to amyotrophic lateral sclerosis progression.Free radical biology & medicine · 2026Article
- Oxeiptosis - potential in cancer treatment?Expert reviews in molecular medicine · 2026Review
- Reactive carbonyl species in health and chronic disease: from methylglyoxal to an integrative network of metabolic regulation.Cardiovascular diabetology · 2026Review
- Progress in the Cross-Organ Biomarker oxLDL in Promoting Pathological Neovascular Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- Review
- Fatty liver reexamined choline and mitochondrial toxin amelioration.World journal of biological chemistry · 2025Review
- Optimizing Membrane Composition With C15 and Choline: A Novel Hypothesis to Mitigate Cancer Risk.Cureus · 2025Review
- NOX-NOS crosstalk in the liver-brain axis: Novel insights for redox regulation and neurodegenerative diseases.Redox biology · 2025Review
- Historical rise of cancer and dietary linoleic acid: Mechanisms and therapeutic strategies.World journal of clinical oncology · 2025Review
- Integrative cardiovascular disease therapy: Linoleic acid restriction, enhanced external counterpulsation, and emerging nanotherapies.World journal of cardiology · 2025Review
- Western Diet and Cognitive Decline: A Hungarian Perspective-Implications for the Design of the Semmelweis Study.Nutrients · 2025Review
- Increasing Life Expectancy with Plant Polyphenols: Lessons from the Mediterranean and Japanese Diets.Molecules (Basel, Switzerland) · 2025Review
- Depolymerization and Oxidation Events in Used Frying Oils Under Conditions Simulating Gastric Digestion.Foods (Basel, Switzerland) · 2025Article
- Scars of oxidative stress: protein carbonylation and beta cell dysfunction in diabetes.Frontiers in endocrinology · 2025Review
- 4-HNE-induced cellular dysfunction from lipid peroxidation: a potential therapeutic target in diabetic cardiomyopathy.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Excessive consumption of vegetable oils such as soybean and canolla oils containing ω-6 polyunsaturated fatty acids is considered one of the most important epidemiological factors leading to the progression of lifestyle-related diseases. However, the underlying mechanism of vegetable-oil-induced organ damage is incompletely elucidated. Since proopiomelanocortin (POMC) neurons in the hypothalamus are related to the control of appetite and energy expenditure, their cell degeneration/death is crucial for the occurrence of obesity. In patients with metabolic syndrome, saturated fatty acids, especially palmitate, are used as an energy source. Since abundant reactive oxygen species are produced during β-oxidation of the palmitate in mitochondria, an increased amount of 4-hydroxy-2-nonenal (4-HNE) is endogenously generated from linoleic acids constituting cardiolipin of the inner membranes. Further, due to the daily intake of deep-fried foods and/or high-fat diets cooked using vegetable oils, exogenous 4-HNE being generated via lipid peroxidation during heating is incorporated into the blood. By binding with atheromatous and/or senile plaques, 4-HNE inactivates proteins via forming hybrid covalent chemical addition compounds and causes cellular dysfunction and tissue damage by the specific oxidation carbonylation. 4-HNE overstimulates G-protein-coupled receptors to induce abnormal Ca
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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.