ArticleAutophagy2015
Thyroid hormone induction of mitochondrial activity is coupled to mitophagy via ROS-AMPK-ULK1 signaling.
Article in Autophagy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 1 of them a synthesis that pooled it.
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Who cites it
119 citing papers in PubMed, 1 synthesis or guideline pooled it, 203 citations in OpenAlex.
- Phytochemicals regulate cancer metabolism through modulation of the AMPK/PGC-1α signaling pathway.BMC cancer · 2024Pooled it
- Mitophagy in cisplatin-induced kidney injury: regulatory mechanisms and therapeutic targets.Annals of medicine · 2026Review
- Mitochondrial dysfunction in urologic disease.Prostate cancer and prostatic diseases · 2026Review
- Engineered levothyroxine dry powder for inhalation to treat idiopathic pulmonary fibrosis.Drug delivery and translational research · 2026Article
- Mechanisms and Therapeutic Potential of Targeting Mitophagy in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Vutiglabridin overcomes the GLP-1 RA-associated weight-loss plateau to achieve normal body weight.International journal of obesity (2005) · 2026Article
- Inflammatory and hormonal crosstalk linking rheumatic fever to chronic valvular heart disease.Molecular biology reports · 2026Review
- Novel bile salt analogs reduce lipid accumulation in liver cells with potential to treat both metabolic dysfunction-associated steatotic liver disease and Clostridioides difficile infection.bioRxiv : the preprint server for biology · 2026Article
- Non-thyroidal Illness Syndrome as an Adaptive Longevity Program: Reframing Low T3 in Acute and Chronic Disease.Cureus · 2026Review
- Thyroid Hormone T3 Induces DNA Damage Response in Breast Cancer Cells.International journal of molecular sciences · 2026Article
- Computational assessment of the relationship between metabolism and histone methylation in cancer cells.PloS one · 2026Article
- Plant-derived nutritional components in thyroid disease-related neuropsychiatric disorders: mechanistic insights and advances.Frontiers in nutrition · 2026Review
- Long-term exposure to low concentrations of ambient benzene with incident thyroid dysfunction and the mediating role of accelerated biological aging.Frontiers in public health · 2026Article
- Resmetirom, the first FDA-approved drug for MASH: From drug discovery and action mechanisms to clinical trials.Archives of pharmacal research · 2025Review
- High-Resolution Spatiotemporal Mapping of Cerebral Metabolism During Middle-Cerebral-Artery Occlusion/Reperfusion Progression: Preliminary Insights.Biomolecules · 2025Article
- Resmetirom: The First FDA-Approved Drug for Metabolic Dysfunction-Associated Steatohepatitis (MASH) with a Perspective on Precision Medicine.Clinical drug investigation · 2025Review
- MASH: the nexus of metabolism, inflammation, and fibrosis.The Journal of clinical investigation · 2025Review
- TTK promotes mitophagy by regulating ULK1 phosphorylation and pre-mRNA splicing to inhibit mitochondrial apoptosis in bladder cancer.Cell death and differentiation · 2025Article
- Serum metabolomics reveals systemic metabolic alterations of Graves' disease before and after antithyroid drug treatment.Endocrine connections · 2025Article
- Exploring the potential regulation of DUOX in thyroid hormone‑autophagy signaling via IGF‑1 in the skeletal muscle (Review).Biomedical reports · 2025Review
59 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Currently, there is limited understanding about hormonal regulation of mitochondrial turnover. Thyroid hormone (T3) increases oxidative phosphorylation (OXPHOS), which generates reactive oxygen species (ROS) that damage mitochondria. However, the mechanism for maintenance of mitochondrial activity and quality control by this hormone is not known. Here, we used both in vitro and in vivo hepatic cell models to demonstrate that induction of mitophagy by T3 is coupled to oxidative phosphorylation and ROS production. We show that T3 induction of ROS activates CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, β) mediated phosphorylation of PRKAA1/AMPK (5' AMP-activated protein kinase), which in turn phosphorylates ULK1 (unc-51 like autophagy activating kinase 1) leading to its mitochondrial recruitment and initiation of mitophagy. Furthermore, loss of ULK1 in T3-treated cells impairs both mitophagy as well as OXPHOS without affecting T3 induced general autophagy/lipophagy. These findings demonstrate a novel ROS-AMPK-ULK1 mechanism that couples T3-induced mitochondrial turnover with activity, wherein mitophagy is necessary not only for removing damaged mitochondria but also for sustaining efficient OXPHOS.
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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.