ArticleBiochimica et biophysica acta2013
Regulation of autophagic flux by dynein-mediated autophagosomes trafficking in mouse coronary arterial myocytes.
Article in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Recycle, repair, recover: the role of autophagy in modulating skeletal muscle repair and post-exercise recovery.Bioscience reports · 2025Review
- Impaired autophagic flux and dedifferentiation in podocytes lacking Asah1 gene: Role of lysosomal TRPML1 channel.Biochimica et biophysica acta. Molecular cell research · 2023Article
- Dync1li1 is required for the survival of mammalian cochlear hair cells by regulating the transportation of autophagosomes.PLoS genetics · 2022Article
- Regulation of exosome release by lysosomal acid ceramidase in coronary arterial endothelial cells: Role of TRPML1 channel.Current topics in membranes · 2022Article
- Arterial Medial Calcification through Enhanced small Extracellular Vesicle Release in Smooth Muscle-Specific Asah1 Gene Knockout Mice.Scientific reports · 2020Article
- Macrophage autophagy regulates mitochondria-mediated apoptosis and inhibits necrotic core formation in vulnerable plaques.Journal of cellular and molecular medicine · 2020Article
- Inhibitory effects of growth differentiation factor 11 on autophagy deficiency-induced dedifferentiation of arterial smooth muscle cells.American journal of physiology. Heart and circulatory physiology · 2019Article
- Finding the Middle Ground for Autophagic Fusion Requirements.Trends in cell biology · 2018Review
- A STRIPAK complex mediates axonal transport of autophagosomes and dense core vesicles through PP2A regulation.The Journal of cell biology · 2017Article
- Contribution of p62 to Phenotype Transition of Coronary Arterial Myocytes with Defective Autophagy.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2017Article
- Cardiac arrest triggers hippocampal neuronal death through autophagic and apoptotic pathways.Scientific reports · 2016Article
- A molecular mechanism to regulate lysosome motility for lysosome positioning and tubulation.Nature cell biology · 2016Article
- Differential cytotoxic effects of 7-dehydrocholesterol-derived oxysterols on cultured retina-derived cells: Dependence on sterol structure, cell type, and density.Experimental eye research · 2016Article
- Regulation of dynein-mediated autophagosomes trafficking by ASM in CASMCs.Frontiers in bioscience (Landmark edition) · 2016Article
- Enhancement of dynein-mediated autophagosome trafficking and autophagy maturation by ROS in mouse coronary arterial myocytes.Journal of cellular and molecular medicine · 2014Article
- Control of autophagy maturation by acid sphingomyelinase in mouse coronary arterial smooth muscle cells: protective role in atherosclerosis.Journal of molecular medicine (Berlin, Germany) · 2014Article
- Defective autophagosome trafficking contributes to impaired autophagic flux in coronary arterial myocytes lacking CD38 gene.Cardiovascular research · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Autophagic flux is an important process during autophagy maturation in coronary arterial myocytes (CAMs). Here, we defined the role and molecular mechanism of the motor protein dynein in the regulation of autophagic flux in CAMs. In mouse CAMs, dynein protein is abundantly expressed. Pharmacological or genetic inhibition of dynein activity dramatically enhanced 7-ketocholesterol (7-Ket)-induced expression of the autophagic marker LC3B and increased the cellular levels of p62, a selective substrate for autophagy. Inhibition of dynein activity increased 7-Ket-induced formation of autophagosomes (APs), but reduced the number of autophagolysosomes (APLs) in CAMs. Furthermore, 7-Ket increased the fusion of APs with lysosomes and the velocity of APs movement in mouse CAMs, which was abolished when the dynein activity in these cells was inhibited. Interestingly, 7-Ket increased lysosomal Ca(2+) release and stimulated dynein ATPase activity, both of which were abolished by NAADP antagonists, NED-19 and PPADS. Taken together, our data suggest that NAADP-mediated Ca(2+) release plays a crucial role in regulating dynein activity, which mediates APs trafficking and fusion with lysosomes to form APLs thus regulating autophagic flux in CAMs under atherogenic stimulation.
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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.