ArticleMedical review (2021)2021
Sympatho-adrenergic mechanisms in heart failure: new insights into pathophysiology.
Article in Medical review (2021), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Grief-Related Chest Pain: A Review, Conceptual Analysis, and Integrative Model.Psychophysiology · 2026Pooled it
- Biased signaling of β2-adrenergic receptor in physiological and pathological states.Cellular & molecular biology letters · 2026Review
- Networked Pathological Mechanisms of Central Sympathetic Nervous System Regulation in Heart Failure and Novel Paradigms for Targeted Intervention.International journal of molecular sciences · 2026Review
- Cardiomyopathy characterizing and heart failure risk predicting by echocardiography and pathoanatomy in aged male mice.Physiological reports · 2024Article
- Protective Effect of Uridine on Structural and Functional Rearrangements in Heart Mitochondria after a High-Dose Isoprenaline Exposure Modelling Stress-Induced Cardiomyopathy in Rats.International journal of molecular sciences · 2023Article
- Cell-cell crosstalk in the heart.Medical review (2021) · 2021Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The sympathetic nervous system is activated in the setting of heart failure (HF) to compensate for hemodynamic instability. However, acute sympathetic surge or sustained high neuronal firing rates activates β-adrenergic receptor (βAR) signaling contributing to myocardial remodeling, dysfunction and electrical instability. Thus, sympatho-βAR activation is regarded as a hallmark of HF and forms pathophysiological basis for β-blocking therapy. Building upon earlier research findings, studies conducted in the recent decades have significantly advanced our understanding on the sympatho-adrenergic mechanism in HF, which forms the focus of this article. This review notes recent research progress regarding the roles of cardiac β
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Registered trials
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