ReviewFrontiers in cell and developmental biology2015
Dysfunctional mitochondrial bioenergetics and the pathogenesis of hepatic disorders.
Review in Frontiers in cell and developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 123 citations in OpenAlex.
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- Curcumin attenuates di(2-ethylhexyl) phthalate-induced hepatic injury in chicks via oxidative stress, glycolysis, and PANoptosis-related signaling.Poultry science · 2026Article
- Exercise-Induced Hepatic Mitochondrial Reprogramming Across Muscle-Gut-Thyroid Axes in MASLD/MASH.International journal of molecular sciences · 2026Review
- The pivotal role of mitochondria in the pathogenesis and treatment of liver failure: a comprehensive review.Molecular and cellular biochemistry · 2026Review
- Complex I Modulator BI4500 Reduces MASH by Limiting Oxidative Stress and Reprogramming Lipid Metabolism via AMPK in MCD Rats.Antioxidants (Basel, Switzerland) · 2026Article
- Novel therapeutic strategies targeting mitochondrial quality control for metabolic dysfunction-associated steatotic liver disease.Frontiers in physiology · 2026Review
- Mitochondrial DNA Damage and Histological Features in Liver Tissue of Azoxymethane-TreatedBiomolecules · 2025Article
- Lipid metabolism orchestrates liver regeneration: an integrated metabolic network.Journal of translational medicine · 2025Review
- Effects of Diet and Exercise on Mitochondrial Health in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): Role of Ceramides.Nutrients · 2025Review
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- Research Progress of Liver Cancer Recurrence Based on Energy Metabolism of Liver Cancer Stem Cells.Journal of hepatocellular carcinoma · 2025Review
- Alcohol and Hepatocellular Carcinoma.Clinics in liver disease · 2024Review
- Mitochondrial heterogeneity and adaptations to cellular needs.Nature cell biology · 2024Review
- Zaluzanin C Alleviates Inflammation and Lipid Accumulation in Kupffer Cells and Hepatocytes by Regulating Mitochondrial ROS.Molecules (Basel, Switzerland) · 2023Article
- Recent progress in understanding mitokines as diagnostic and therapeutic targets in hepatocellular carcinoma.World journal of clinical cases · 2023Review
- Involvement of necroptosis in the selective toxicity of the natural compound (±) gossypol on squamous skin cancer cells in vitro.Archives of toxicology · 2023Article
- Mitofusin-2 gene polymorphisms and metabolic dysfunction associated fatty liver disease: a case-control study in a Chinese population.The Journal of international medical research · 2023Article
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- Beneficial Effects of Viable and Heat-InactivatedAntioxidants (Basel, Switzerland) · 2023Article
- Hepatic expression of sodium-glucose cotransporter 2 (SGLT2) in patients with chronic liver disease.Medical molecular morphology · 2022Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The liver is involved in a variety of critical biological functions including the homeostasis of glucose, fatty acids, amino acids, and the synthesis of proteins that are secreted in the blood. It is also at the forefront in the detoxification of noxious metabolites that would otherwise upset the functioning of the body. As such, this vital component of the mammalian system is exposed to a notable quantity of toxicants on a regular basis. It therefore comes as no surprise that there are over a hundred disparate hepatic disorders, encompassing such afflictions as fatty liver disease, hepatitis, and liver cancer. Most if not all of liver functions are dependent on energy, an ingredient that is primarily generated by the mitochondrion, the power house of all cells. This organelle is indispensable in providing adenosine triphosphate (ATP), a key effector of most biological processes. Dysfunctional mitochondria lead to a shortage in ATP, the leakage of deleterious reactive oxygen species (ROS), and the excessive storage of fats. Here we examine how incapacitated mitochondrial bioenergetics triggers the pathogenesis of various hepatic diseases. Exposure of liver cells to detrimental environmental hazards such as oxidative stress, metal toxicity, and various xenobiotics results in the inactivation of crucial mitochondrial enzymes and decreased ATP levels. The contribution of the latter to hepatic disorders and potential therapeutic cues to remedy these conditions are elaborated.
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