ReviewJournal of biomedical science2019
Molecular functions and clinical impact of thyroid hormone-triggered autophagy in liver-related diseases.
Review in Journal of biomedical science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 2 syntheses or guidelines pooled it, 89 citations in OpenAlex.
- Pooled it
- Evidence on the link between hypothyroidism and non-alcoholic fatty liver disease: an updated systematic review.BMC endocrine disorders · 2025Pooled it
- Thyroid hormone deprivation creates an immunological signature in the mouse liver, involving Kupffer cell presentation as the mouse ages.Endocrine · 2026Article
- Phloretin Attenuates Cancer Cachexia-Induced Skeletal Muscle Wasting Associated with the Modulation of STAT3 Signaling.Biomedicines · 2026Article
- Novel biomarkers for alcohol-associated liver disease and their implications across clinical settings.Clinical and molecular hepatology · 2026Review
- NAFLD and Hypothyroidism: Deciphering Pivotal Genetic Variants, Cellular Expression Landscapes, and Spatial Architectures.International journal of molecular sciences · 2026Article
- Hypothyroidism and the risk of liver-related events in patients with metabolic dysfunction-associated steatotic liver disease.Clinical and molecular hepatology · 2026Article
- Mitochondrial dysfunction in hepatocellular carcinoma: from metabolism to targeted therapies.Molecular and cellular biochemistry · 2025Review
- Induction of Autophagy as a Therapeutic Breakthrough for NAFLD: Current Evidence and Perspectives.Biology · 2025Review
- Endurance Training Alleviates Metabolic-Associated Fatty-Liver Disease (MAFLD)-Related Testicular Impairments via Endoplasmic Reticulum Stress Regulation.Journal of clinical laboratory analysis · 2025Article
- Predictors of poor prognosis in long-term survivors of differentiated thyroid cancer with psychiatric disorders.World journal of psychiatry · 2025Article
- Risk factors and prediction model of metabolic disorders in adult patients with pituitary stalk interruption syndrome.Scientific reports · 2025Article
- Hypothyroidism/subclinical hypothyroidism and metabolic dysfunction-associated steatotic liver disease: advances in mechanism and treatment.Lipids in health and disease · 2025Review
- ECM remodeling in hypothyroidism-associated MAFLD: mechanisms, clinical relevance, and therapeutic targets.Frontiers in immunology · 2025Review
- Targeting THR-β for MASLD: Mechanisms and Drug Development.Drug design, development and therapy · 2025Review
- Ameliorative effect of ferulic acid on thyroid dysfunction against propyl-thiouracil induced hypothyroid rats.Endocrine · 2024Article
- Melissa officinalis extract palliates redox imbalance and inflammation associated with hyperthyroidism-induced liver damage by regulating Nrf-2/ Keap-1 gene expression in γ-irradiated rats.BMC complementary medicine and therapies · 2024Article
- The role of autophagy in Graves disease: knowns and unknowns.Frontiers in cell and developmental biology · 2024Review
- Autophagy modulates physiologic and adaptive response in the liver.Liver research (Beijing, China) · 2023Review
- Autophagy and Senescence: The Molecular Mechanisms and Implications in Liver Diseases.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
5 authors at 3 institutions in 1 country.
Funding
Abstract
The liver is controlled by several metabolic hormones, including thyroid hormone, and characteristically displays high lysosomal activity as well as metabolic stress-triggered autophagy, which is stringently regulated by the levels of hormones and metabolites. Hepatic autophagy provides energy through catabolism of glucose, amino acids and free fatty acids for starved cells, facilitating the generation of new macromolecules and maintenance of the quantity and quality of cellular organelles, such as mitochondria. Dysregulation of autophagy and defective mitochondrial homeostasis contribute to hepatocyte injury and liver-related diseases, such as non-alcoholic fatty liver disease (NAFLD) and liver cancer.Thyroid hormones (TH) mediate several critical physiological processes including organ development, cell differentiation, metabolism and cell growth and maintenance. Accumulating evidence has revealed dysregulation of cellular TH activity as the underlying cause of several liver-related diseases, including alcoholic or non-alcoholic fatty liver disease and liver cancer. Data from epidemiologic, animal and clinical studies collectively support preventive functions of THs in liver-related diseases, highlighting the therapeutic potential of TH analogs. Elucidation of the molecular mechanisms and downstream targets of TH should thus facilitate the development of therapeutic strategies for a number of major public health issues.Here, we have reviewed recent studies focusing on the involvement of THs in hepatic homeostasis through induction of autophagy and their implications in liver-related diseases. Additionally, the potential underlying molecular pathways and therapeutic applications of THs in NAFLD and HCC are discussed.
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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.