ArticleCirculation research2026
Mitophagy Facilitates Cytosolic Proteostasis to Preserve Cardiac Function.
Article in Circulation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Mitochondria Take Up and Dispose of Cytosolic Protein Aggregates.Circulation research · 2026Article
- A Micro-Engineered Heart Tissue Model of Desmin-related Cardiomyopathy Caused by Mutant αB Crystallin.bioRxiv : the preprint server for biology · 2025Article
- Beyond autophagic flux: selective autophagy adaptors and cargo prioritization in cardiac disease.Cardiology plusReview
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Authors and funding
18 authors.
Funding
Abstract
backgroundProtein quality control is critical for maintaining sarcomere structure and function in cardiomyocytes. Mutations in protein quality control pathway proteins, namely, CRYAB-R120G (crystallin alpha B with arginine to glycine at position 120) and BAG3-P209L (Bcl-2-associated athanogene 3 with proline to lysine at position 209), induce protein aggregates and cardiomyopathy in humans. Novel observations in yeast demonstrate mitochondrial uptake of cytosolic protein aggregates. We hypothesized that mitochondrial uptake of cytosolic protein aggregates, and their removal by mitophagy, a lysosomal degradative pathway, facilitates cytosolic protein quality control in cardiomyocytes.
methodsMice with inducible cardiac myocyte-specific ablation of TRAF2 (TNF receptor-associated factor 2; TRAF2-icKO [inducible conditional knockout]), which impairs mitophagy, were assessed for protein aggregates with biochemical fractionation and super-resolution imaging. Human-induced pluripotent stem cell-derived cardiomyocytes with
resultsTRAF2-icKO mice demonstrate accumulation of mitochondrial and cytosolic protein aggregates and DESMIN mislocalization to protein aggregates.
conclusionsStimulation of mitophagy in cardiomyocytes facilitates removal of cytosolic protein aggregates as a mechanism to ameliorate proteotoxic cardiomyopathy.
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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.