ReviewInternational journal of molecular sciences2021
Remodeling of Mitochondrial Plasticity: The Key Switch from NAFLD/NASH to HCC.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 51 citations in OpenAlex.
- Polyphenol-RichMolecules (Basel, Switzerland) · 2026Article
- Metabolic Pathways Linking Atherosclerotic Cardiovascular Disease With Metabolic Dysfunction-Associated Steatotic Liver Disease.Current atherosclerosis reports · 2026Review
- Article
- Mitochondrial Dysfunction in MASLD: Evidence in Dietary Models and Potential Therapeutic Interventions.Biochemistry research international · 2026Review
- The Role of Mitochondrial Complexes in Liver Diseases.Journal of clinical and translational hepatology · 2025Review
- Artificial intelligence as a ploy to delve into the intricate link between genetics and mitochondria in patients with MASLD.JHEP reports : innovation in hepatology · 2025Article
- Exploring multiorgan mitochondrial dysfunction in the switch toward progressive MASLD in AMLN mice.iScience · 2025Article
- Lipid Droplet-Organized MDM2-Mediated P53 Degradation: A Metabolic Switch Governing Diet-Driven Tumor Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mitochondrial Dysfunction as a Pathogenesis and Therapeutic Strategy for Metabolic-Dysfunction-Associated Steatotic Liver Disease.International journal of molecular sciences · 2025Review
- Identification of key molecular targets for stachyose in hepatocellular carcinoma: focus on STAT3 and FN1.Frontiers in oncology · 2025Article
- Recent Advances in miRNA-Based Therapy for MASLD/MASH and MASH-Associated HCC.International journal of molecular sciences · 2024Review
- Mechanisms of Non-alcoholic Fatty Liver Disease and Beneficial Effects of Semaglutide: A Review.Cureus · 2024Review
- Review
- Glutamine prevents high-fat diet-induced hepatic lipid accumulation in mice by modulating lipolysis and oxidative stress.Nutrition & metabolism · 2024Article
- Mitochondrial Dysfunction in Metabolic Dysfunction Fatty Liver Disease (MAFLD).International journal of molecular sciences · 2023Review
- Molecular and cellular mechanisms underlying the hepatoprotective role of ghrelin against NAFLD progression.Journal of physiology and biochemistry · 2023Review
- mTOR-dependent loss of PON1 secretion and antiphospholipid autoantibody production underlie autoimmunity-mediated cirrhosis in transaldolase deficiency.Journal of autoimmunity · 2023Article
- Coagulation Dysfunctions in Non-Alcoholic Fatty Liver Disease-Oxidative Stress and Inflammation Relevance.Medicina (Kaunas, Lithuania) · 2023Review
- An immune-related signature for optimizing prognosis prediction and treatment decision of hepatocellular carcinoma.European journal of medical research · 2023Article
- Tumor Mutational Burden for Predicting Prognosis and Therapy Outcome of Hepatocellular Carcinoma.International journal of molecular sciences · 2023Review
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 2 institutions in 1 country.
Funding
Abstract
Hepatocellular carcinoma (HCC) is the most common primary malignancy of the liver and the third-leading cause of cancer-related mortality. Currently, the global burden of nonalcoholic fatty liver disease (NAFLD) has dramatically overcome both viral and alcohol hepatitis, thus becoming the main cause of HCC incidence. NAFLD pathogenesis is severely influenced by lifestyle and genetic predisposition. Mitochondria are highly dynamic organelles that may adapt in response to environment, genetics and epigenetics in the liver ("mitochondrial plasticity"). Mounting evidence highlights that mitochondrial dysfunction due to loss of mitochondrial flexibility may arise before overt NAFLD, and from the early stages of liver injury. Mitochondrial failure promotes not only hepatocellular damage, but also release signals (mito-DAMPs), which trigger inflammation and fibrosis, generating an adverse microenvironment in which several hepatocytes select anti-apoptotic programs and mutations that may allow survival and proliferation. Furthermore, one of the key events in malignant hepatocytes is represented by the remodeling of glucidic-lipidic metabolism combined with the reprogramming of mitochondrial functions, optimized to deal with energy demand. In sum, this review will discuss how mitochondrial defects may be translated into causative explanations of NAFLD-driven HCC, emphasizing future directions for research and for the development of potential preventive or curative strategies.
Indexed as
Identifiers
What Socratic 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 Socratic graph.