ArticleJACC. Basic to translational science2025
Proteostatic Imbalance Drives the Pathogenesis and Age-Related Exacerbation of Heart Failure With Preserved Ejection Fraction.
Article in JACC. Basic to translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Cardiometabolic stress induces HFpEF with impaired bioenergetics and disrupted proteostasis in aged female mice.Journal of molecular and cellular cardiology · 2026Article
- Cardiometabolic Aging Driven by Multi-Organ Crosstalk: Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Metabolic inflexibility across heart failure phenotypes: mechanisms and type-specific therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Heart Failure with Preserved Ejection Fraction as a Multisystem Syndrome: A Mechanistically Anchored Endotype Framework for Precision Therapy.Journal of clinical medicine · 2026Review
- Identification and validation of an interaction between the E3 ubiquitin ligase WWP1 and the Transcriptional Co-Activator WBP2 in the human heart.Biology open · 2026Article
- Unravelling the Pathogenesis of Heart Failure with Preserved Ejection Fraction: The Pivotal Role of Autophagy and Endoplasmic Reticulum Stress.European cardiology · 2026Review
- The Role of Aging in Heart Failure With Preserved Ejection Fraction: Focus on Proteostatic Imbalance.JACC. Basic to translational science · 2025Article
- Heart failure: mechanistic insights and precision therapeutic strategies.Frontiers in cardiovascular medicine · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Heart failure with preserved ejection fraction (HFpEF) is a leading cause of hospitalization and mortality in older adults, yet the role of aging in its pathogenesis remains unclear. Old male mice subjected to chronic metabolic and hypertensive stress (2-hit) developed a more severe HFpEF phenotype compared with young counterparts. We identified that age-related disruptions in protein quality control (PQC) worsens proteostatic stress in HFpEF. Mammalian target of rapamycin complex 1 (mTORC1), a key regulator of PQC, is activated by both aging and 2-hit stress, and cardiac-specific mTORC1 inhibition protects against HFpEF. Our findings highlight the need to integrate aging into preclinical models of HFpEF and suggest targeting PQC as a therapeutic strategy.
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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 Socratic graph.