ReviewExperimental physiology2015
Mechanisms of carotid body chemoreflex dysfunction during heart failure.
Review in Experimental physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 72 citations in OpenAlex.
- Acute inorganic nitrate supplementation and the hypoxic ventilatory response in patients with obstructive sleep apnea.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Trial
- Dyspnea in heart failure: pathophysiology, clinical assessment, and evidence from clinical trials.Heart failure reviews · 2026Review
- Amino acid modulation of the carotid body selectively modulates peripheral chemoreceptor respiratory reflex.The Journal of physiology · 2026Article
- The influence of metaboreflex activation on pulmonary pressure with combined chemoreflex activation in acute and chronic hypoxia.The Journal of physiology · 2026Article
- Targeting ecto-5'-nucleotidase (CD73) and cAMP alleviates carotid body hyperactivity and reduces blood pressure in chronically hypoxic rats.The Journal of physiology · 2026Article
- Obligatory neural feedback control of exercise cardiorespiratory function and performance.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Review
- Chemoreflex function in pulmonary diseases - A review.The Journal of physiology · 2025Review
- Sympathetic Nervous System in Heart Failure: Targets for Treatments.Current hypertension reports · 2025Review
- Translating physiology of the arterial chemoreflex into novel therapeutic interventions targeting carotid bodies in cardiometabolic disorders.The Journal of physiology · 2025Review
- Review
- Article
- Baroreflex and chemoreflex interaction in high-altitude exposure: possible role on exercise performance.Frontiers in physiology · 2024Review
- The Carotid Body "Tripartite Synapse": Role of Gliotransmission.Advances in experimental medicine and biology · 2023Review
- Carotid Body Dysfunction and Mechanisms of Disease.Advances in anatomy, embryology, and cell biology · 2023Article
- Intra-carotid body inter-cellular communication.Journal of the Royal Society of New Zealand · 2023Review
- The effects of P2YFrontiers in physiology · 2023Article
- Clinical determinants and prognostic significance of hypocapnia in acute heart failure.Scientific reports · 2022Article
- The Pathogenesis of Central and Complex Sleep Apnea.Current neurology and neuroscience reports · 2022Review
- GLP-1 (Glucagon-Like Peptide-1) Plays a Role in Carotid Chemoreceptor-Mediated Sympathoexcitation and Hypertension.Circulation research · 2022Article
- Obstructive sleep apnea.Handbook of clinical neurology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
NEW
findingsWhat is the topic of this review? Carotid body chemoreceptor activity is tonically elevated in heart failure and contributes to morbidity due to the reflex activation of sympathetic nerve activity and destabilization of breathing. The potential causes for the enhanced chemoreceptor activation in heart failure are discussed. What advances does it highlight? The role of a chronic reduction in blood flow to the carotid body due to cardiac failure and its impact on signalling pathways in the carotid body is discussed. Recent advances have attracted interest in the potential for carotid body (CB) ablation or desensitization as an effective strategy for clinical treatment and management of cardiorespiratory diseases, including hypertension, heart failure, diabetes mellitus, metabolic syndrome and renal failure. These disease states have in common sympathetic overactivity, which plays an important role in the development and progression of the disease and is often associated with breathing dysregulation, which in turn is likely to mediate or aggravate the autonomic imbalance. Evidence from both chronic heart failure (CHF) patients and animal models indicates that the CB chemoreflex is enhanced in CHF and contributes to the tonic elevation in sympathetic activity and the development of periodic breathing associated with the disease. Although this maladaptive change is likely to derive from altered function at all levels of the reflex arc, a tonic increase in afferent activity from CB glomus cells is likely to be a main driving force. This report focuses on our understanding of mechanisms that alter CB function in CHF and their potential translational impact on treatment of CHF.
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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.