ReviewThe Journal of physiology2020
Neurocardiac regulation: from cardiac mechanisms to novel therapeutic approaches.
Review in The Journal of physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Multimodal, device-based therapeutic targeting of the cardiovascular autonomic nervous system.Nature reviews. Cardiology · 2026Review
- Ex vivo calcium imaging of sympathetic neurons in intact mouse stellate ganglia.Autonomic neuroscience : basic & clinical · 2025Article
- Bioelectronic block of stellate ganglia mitigates pacing-induced heterogeneous release of catecholamine and neuropeptide Y in the infarcted pig heart.The Journal of physiology · 2025Article
- Molecular and cellular neurocardiology in heart disease.The Journal of physiology · 2025Review
- Oxysterols in Central and Peripheral Synaptic Communication.Advances in experimental medicine and biology · 2024Article
- Autonomic control of ventricular function in health and disease: current state of the art.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023Review
- Cholinergic collaterals arising from noradrenergic sympathetic neurons in mice.The Journal of physiology · 2023Article
- What gets on the nerves of cardiac patients? Pathophysiological changes in cardiac innervation.The Journal of physiology · 2022Article
- Cellular basis of learning and memory in the carotid body.Frontiers in synaptic neuroscience · 2022Review
- From Mice to Mainframes: Experimental Models for Investigation of the Intracardiac Nervous System.Journal of cardiovascular development and disease · 2021Review
- The Intrinsic Cardiac Nervous System and Its Role in Cardiac Pacemaking and Conduction.Journal of cardiovascular development and disease · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac sympathetic overactivity is a well-established contributor to the progression of neurogenic hypertension and heart failure, yet the underlying pathophysiology remains unclear. Recent studies have highlighted the importance of acutely regulated cyclic nucleotides and their effectors in the control of intracellular calcium and exocytosis. Emerging evidence now suggests that a significant component of sympathetic overactivity and enhanced transmission may arise from impaired cyclic nucleotide signalling, resulting from compromised phosphodiesterase activity, as well as alterations in receptor-coupled G-protein activation. In this review, we address some of the key cellular and molecular pathways that contribute to sympathetic overactivity in hypertension and discuss their potential for therapeutic targeting.
Indexed as
Identifiers
What OpenQuestion holds
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.