ArticleJACC. Basic to translational science2022
Targeting the Autophagy-Lysosome Pathway in a Pathophysiologically Relevant Murine Model of Reversible Heart Failure.
Article in JACC. Basic to translational science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 22 citations in OpenAlex.
- Cardiac unloading models for myocardial reverse remodeling.Basic research in cardiology · 2026Review
- TFEB Antagonizes Cardiac Hypertrophy and Failure by Enhancing Lysosomal Capacity and Mitochondrial Function.Circulation research · 2026Article
- The UFM1 Conjugation System: A Master Regulator of Cellular Stress Surveillance in Human Disease.Biology · 2026Review
- Upregulation of PPTC7 in brain microvascular endothelial cell aggravates diabetic cognitive dysfunction by impairing PHB2 mediated mitochondrial function.Redox biology · 2026Article
- Asporin Improves Cardiac Myocyte Response to Ischemia and Reperfusion Stress.bioRxiv : the preprint server for biology · 2026Article
- Disulfidptosis in heart failure: an emerging mechanism awaiting exploration.Frontiers in cardiovascular medicine · 2026Review
- B lymphocytes contribute Angiotensin II induced cardiac hypertrophy.Scientific reports · 2025Article
- Dysregulated Redox Signaling and Its Impact on Inflammatory Pathways, Mitochondrial Dysfunction, Autophagy and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Review
- Review
- SGLT2i Therapy Prevents Anthracycline-Induced Cardiotoxicity in a Large Animal Model by Preserving Myocardial Energetics.JACC. CardioOncology · 2025Article
- Unraveling mitochondrial crosstalk: a new frontier in heart failure pathogenesis.Frontiers in cardiovascular medicine · 2025Review
- Sacubitril/valsartan reduces proteasome activation and cardiomyocyte area in an experimental mouse model of hypertrophy.Journal of molecular and cellular cardiology plus · 2024Article
- Multi-omic and multispecies analysis of right ventricular dysfunction.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2024Article
- Assessment of Autophagy Markers Suggests Increased Activity Following LVAD Therapy.JACC. Basic to translational science · 2023Article
- Autophagy in the LVAD-Supported Heart: A Sign of Hope or a Marker of Unloading.JACC. Basic to translational science · 2023Article
- Apolipoprotein M Attenuates Anthracycline Cardiotoxicity and Lysosomal Injury.JACC. Basic to translational science · 2023Article
- Article
- Protein homeostasis in the aged and diseased heart.The journal of cardiovascular aging · 2023Article
- Reduce, Reuse, Recycle…Unloading, Autophagy, and Myocardial Recovery.JACC. Basic to translational science · 2022Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The key biological "drivers" that are responsible for reverse left ventricle (LV) remodeling are not well understood. To gain an understanding of the role of the autophagy-lysosome pathway in reverse LV remodeling, we used a pathophysiologically relevant murine model of reversible heart failure, wherein pressure overload by transaortic constriction superimposed on acute coronary artery (myocardial infarction) ligation leads to a heart failure phenotype that is reversible by hemodynamic unloading. Here we show transaortic constriction + myocardial infarction leads to decreased flux through the autophagy-lysosome pathway with the accumulation of damaged proteins and organelles in cardiac myocytes, whereas hemodynamic unloading is associated with restoration of autophagic flux to normal levels with incomplete removal of damaged proteins and organelles in myocytes and reverse LV remodeling, suggesting that restoration of flux is insufficient to completely restore myocardial proteostasis. Enhancing autophagic flux with adeno-associated virus 9-transcription factor EB resulted in more favorable reverse LV remodeling in mice that had undergone hemodynamic unloading, whereas overexpressing transcription factor EB in mice that have not undergone hemodynamic unloading leads to increased mortality, suggesting that the therapeutic outcomes of enhancing autophagic flux will depend on the conditions in which flux is being studied.
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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.