The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Intracellular Protein Aggregation Is a Proximal Trigger of Cardiomyocyte Autophagy
Open accessAbstract
Background— Recent reports demonstrate that multiple forms of cardiovascular stress, including pressure overload, chronic ischemia, and infarction-reperfusion injury, provoke an increase in autophagic activity in cardiomyocytes. However, nothing is known regarding molecular events that stimulate autophagic activity in stressed myocardium. Because autophagy is a highly conserved process through which damaged proteins and organelles can be degraded, we hypothesized that stress-induced protein aggregation is a proximal trigger of cardiomyocyte autophagy. Methods and Results— Here, we report that pressure overload promotes accumulation of ubiquitinated protein aggregates in the left ventricle, development of aggresome-like structures, and a corresponding induction of autophagy. To test for causal links, we induced protein accumulation in cultured cardiomyocytes by inhibiting proteasome activity, finding that aggregation of polyubiquitinated proteins was sufficient to induce cardiomyocyte autophagy. Furthermore, attenuation of autophagic activity dramatically enhanced both aggresome size and abundance, consistent with a role for autophagic activity in protein aggregate clearance. Conclusions— We conclude that protein aggregation is a proximal trigger of cardiomyocyte autophagy and that autophagic activity functions to attenuate aggregate/aggresome formation in heart. Findings reported here are the first to demonstrate that protein aggregation occurs in response to hemodynamic stress, situating pressure-overload heart disease in the category of proteinopathies.
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Cites
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Cited by
Regulation of Mammalian Autophagy in Physiology and Pathophysiology
Ravikumar, B., Sarkar, S., Davies, J. E., Futter, M., Garcia-Arencibia, M., Green-Thompson, Z. W., Jimenez-Sanchez, M., Korolchuk, V. I., Lichtenberg, M., Luo, S., et al. (2010) · Physiological Reviews · doi:10.1152/physrev.00030.2009 · Cited by 1,727
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Mst1 inhibits autophagy by promoting the interaction between Beclin1 and Bcl-2
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Crosstalk Between Mammalian Autophagy and the Ubiquitin-Proteasome System
Kocaturk, N. M., & Gozuacik, D. (2018) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2018.00128 · Cited by 419
Autophagy in Ischemic Heart Disease
Gustafsson, A. B., & Gottlieb, R. A. (2009) · Circulation Research · doi:10.1161/circresaha.108.187427 · Cited by 395
Metadata
- Authors
- Tannous, P., Zhu, H., Nemchenko, A., Berry, J. M., Johnstone, J. L., Shelton, J. M., Miller, F. J., Rothermel, B. A., & Hill, J. A.
- Venue
- Circulation
- Published
- 2008-06-17
- Volume
- 117
- Issue
- 24
- Pages
- 3070-3078
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2062629975
- Cited by
- 248
- References
- 13
- FWCI
- 12.92
- Type
- journal article
- Language
- en
- Open access
- green
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- Tannous, P., Zhu, H., Nemchenko, A., Berry, J. M., Johnstone, J. L., Shelton, J. M., Miller, F. J., Rothermel, B. A., & Hill, J. A. (2008). Intracellular Protein Aggregation Is a Proximal Trigger of Cardiomyocyte Autophagy. Circulation. https://doi.org/10.1161/circulationaha.107.763870
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
