ArticleAmerican journal of physiology. Heart and circulatory physiology2013
AMPK attenuates microtubule proliferation in cardiac hypertrophy.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 55 citations in OpenAlex.
- TFEB Antagonizes Cardiac Hypertrophy and Failure by Enhancing Lysosomal Capacity and Mitochondrial Function.Circulation research · 2026Article
- Review
- Runx2 Regulated Airway Homeostasis Is Disrupted in Asthma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- ArfGAP with Dual Pleckstrin Homology Domains 2 Promotes Hypertrophy of Cultured Neonatal Cardiomyocytes.International journal of molecular sciences · 2025Article
- Article
- Dysfunctional cardiomyocyte signalling and heart disease.Current opinion in cell biology · 2025Review
- Syringaldehyde Alleviates Cardiac Hypertrophy Induced by Hyperglycemia in H9c2 Cells Through GLP-1 Receptor Signals.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Mechano-energetic uncoupling in hypertrophic cardiomyopathy: Pathophysiological mechanisms and therapeutic opportunities.Journal of molecular and cellular cardiology plus · 2023Review
- Intermittent Fasting Activates AMP-Kinase to Restructure Right Ventricular Lipid Metabolism and Microtubules.JACC. Basic to translational science · 2023Article
- Metabolic Changes in Cardiac Aging.Reviews in cardiovascular medicine · 2023Review
- The microtubule cytoskeleton in cardiac mechanics and heart failure.Nature reviews. Cardiology · 2022Review
- Tubulin acetylation increases cytoskeletal stiffness to regulate mechanotransduction in striated muscle.The Journal of general physiology · 2021Article
- The role of SIRT2 in vascular-related and heart-related diseases: A review.Journal of cellular and molecular medicine · 2021Review
- Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy.Biological research · 2021Article
- Natural AMPK Activators in Cardiovascular Disease Prevention.Frontiers in pharmacology · 2021Review
- Aging, Osteo-Sarcopenia, and Musculoskeletal Mechano-Transduction.Frontiers in rehabilitation sciences · 2021Article
- Microtubules Increase Diastolic Stiffness in Failing Human Cardiomyocytes and Myocardium.Circulation · 2020Article
- Cardiac microtubules in health and heart disease.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Adenosine kinase attenuates cardiomyocyte microtubule stabilization and protects against pressure overload-induced hypertrophy and LV dysfunction.Journal of molecular and cellular cardiology · 2019Article
- WIPI1 is a conserved mediator of right ventricular failure.JCI insight · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Cell hypertrophy requires increased protein synthesis and expansion of the cytoskeletal networks that support cell enlargement. AMPK limits anabolic processes, such as protein synthesis, when energy supply is insufficient, but its role in cytoskeletal remodeling is not known. Here, we examined the influence of AMPK in cytoskeletal remodeling during cardiomyocyte hypertrophy, a clinically relevant condition in which cardiomyocytes enlarge but do not divide. In neonatal cardiomyocytes, activation of AMPK with 5-aminoimidazole carboxamide ribonucleotide (AICAR) or expression of constitutively active AMPK (CA-AMPK) attenuated cell area increase by hypertrophic stimuli (phenylephrine). AMPK activation had little effect on intermediate filaments or myofilaments but dramatically reduced microtubule stability, as measured by detyrosinated tubulin levels and cytoskeletal tubulin accumulation. Importantly, low-level AMPK activation limited cell expansion and microtubule growth independent of mTORC1 or protein synthesis repression, identifying a new mechanism by which AMPK regulates cell growth. Mechanistically, AICAR treatment increased Ser-915 phosphorylation of microtubule-associated protein 4 (MAP4), which reduces affinity for tubulin and prevents stabilization of microtubules (MTs). RNAi knockdown of MAP4 confirmed its critical role in cardiomyocyte MT stabilization. In support of a pathophysiological role for AMPK regulation of cardiac microtubules, AMPK α2 KO mice exposed to pressure overload (transverse aortic constriction; TAC) demonstrated reduced MAP4 phosphorylation and increased microtubule accumulation that correlated with the severity of contractile dysfunction. Together, our data identify the microtubule cytoskeleton as a sensitive target of AMPK activity, and the data suggest a novel role for AMPK in limiting accumulation and densification of microtubules that occurs in response to hypertrophic stress.
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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.