Cardiac TRPV1 afferent signaling promotes arrhythmogenic ventricular remodeling after myocardial infarction Article Swipe
Koji Yoshie
,
Pradeep S. Rajendran
,
Louis Massoud
,
Janki Mistry
,
Mohammed Amer Swid
,
Xiaohui Wu
,
Tamer Sallam
,
Rui Zhang
,
Joshua I. Goldhaber
,
Siamak Salavatian
,
Olujimi A. Ajijola
·
YOU?
·
· 2019
· Open Access
·
· DOI: https://doi.org/10.1172/jci.insight.124477
YOU?
·
· 2019
· Open Access
·
· DOI: https://doi.org/10.1172/jci.insight.124477
Chronic sympathoexcitation is implicated in ventricular arrhythmogenesis (VAs) following myocardial infarction (MI), but the critical neural pathways involved are not well understood. Cardiac adrenergic function is partly regulated by sympathetic afferent reflexes, transduced by spinal afferent fibers expressing the transient receptor potential cation subfamily V member 1 (TRPV1) channel. The role of chronic TRPV1 afferent signaling in VAs is not known. We hypothesized that persistent TRPV1 afferent neurotransmission promotes VAs after MI. Using epicardial resiniferatoxin (RTX) to deplete cardiac TRPV1-expressing fibers, we dissected the role of this neural circuit in VAs after chronic MI in a porcine model. We examined the underlying mechanisms using molecular approaches, IHC, in vitro and in vivo cardiac electrophysiology, and simultaneous cardioneural mapping. Epicardial RTX depleted cardiac TRPV1 afferent fibers and abolished functional responses to TRPV1 agonists. Ventricular tachycardia/fibrillation (VT/VF) was readily inducible in MI subjects by programmed electrical stimulation or cesium chloride administration; however, TRPV1 afferent depletion prevented VT/VF induced by either method. Mechanistically, TRPV1 afferent depletion did not alter cardiomyocyte action potentials and calcium transients, the expression of ion channels, or calcium handling proteins. However, it attenuated fibrosis and mitigated electrical instability in the scar border zone. In vivo recordings of cardiovascular-related stellate ganglion neurons (SGNs) revealed that MI enhances SGN function and disrupts integrated neural processing. Depleting TRPV1 afferents normalized these processes. Taken together, these data indicate that, after MI, TRPV1 afferent-induced adrenergic dysfunction promotes fibrosis and adverse cardiac remodeling, and it worsens border zone electrical heterogeneity, resulting in electrically unstable ventricular myocardium. We propose targeting TRPV1-expressing afferent to reduce VT/VF following MI.
Related Topics
Concepts
TRPV1
Resiniferatoxin
Internal medicine
Medicine
Endocrinology
Transient receptor potential channel
Cardiology
Chemistry
Neuroscience
Receptor
Biology
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1172/jci.insight.124477
- http://insight.jci.org/articles/view/124477/files/pdf
- OA Status
- gold
- Cited By
- 71
- References
- 32
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W2995658260
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W2995658260Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1172/jci.insight.124477Digital Object Identifier
- Title
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Cardiac TRPV1 afferent signaling promotes arrhythmogenic ventricular remodeling after myocardial infarctionWork title
- Type
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articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2019Year of publication
- Publication date
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2019-12-17Full publication date if available
- Authors
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Koji Yoshie, Pradeep S. Rajendran, Louis Massoud, Janki Mistry, Mohammed Amer Swid, Xiaohui Wu, Tamer Sallam, Rui Zhang, Joshua I. Goldhaber, Siamak Salavatian, Olujimi A. AjijolaList of authors in order
- Landing page
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https://doi.org/10.1172/jci.insight.124477Publisher landing page
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https://insight.jci.org/articles/view/124477/files/pdfDirect link to full text PDF
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
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https://insight.jci.org/articles/view/124477/files/pdfDirect OA link when available
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TRPV1, Resiniferatoxin, Internal medicine, Medicine, Endocrinology, Transient receptor potential channel, Cardiology, Chemistry, Neuroscience, Receptor, BiologyTop concepts (fields/topics) attached by OpenAlex
- Cited by
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71Total citation count in OpenAlex
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2025: 7, 2024: 17, 2023: 13, 2022: 20, 2021: 9Per-year citation counts (last 5 years)
- References (count)
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32Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.not | 19, 59, 164 |
| abstract_inverted_index.the | 13, 38, 83, 100, 172, 190 |
| abstract_inverted_index.was | 135 |
| abstract_inverted_index.IHC, | 106 |
| abstract_inverted_index.data | 223 |
| abstract_inverted_index.role | 50, 84 |
| abstract_inverted_index.scar | 191 |
| abstract_inverted_index.that | 63, 204 |
| abstract_inverted_index.this | 86 |
| abstract_inverted_index.vivo | 111, 195 |
| abstract_inverted_index.well | 20 |
| abstract_inverted_index.zone | 242 |
| abstract_inverted_index.(MI), | 11 |
| abstract_inverted_index.(RTX) | 75 |
| abstract_inverted_index.(VAs) | 7 |
| abstract_inverted_index.TRPV1 | 53, 65, 122, 130, 150, 160, 215, 228 |
| abstract_inverted_index.Taken | 220 |
| abstract_inverted_index.Using | 72 |
| abstract_inverted_index.VT/VF | 154, 258 |
| abstract_inverted_index.after | 70, 91, 226 |
| abstract_inverted_index.alter | 165 |
| abstract_inverted_index.that, | 225 |
| abstract_inverted_index.these | 218, 222 |
| abstract_inverted_index.using | 103 |
| abstract_inverted_index.vitro | 108 |
| abstract_inverted_index.zone. | 193 |
| abstract_inverted_index.(SGNs) | 202 |
| abstract_inverted_index.action | 167 |
| abstract_inverted_index.border | 192, 241 |
| abstract_inverted_index.cation | 42 |
| abstract_inverted_index.cesium | 146 |
| abstract_inverted_index.either | 157 |
| abstract_inverted_index.fibers | 36, 124 |
| abstract_inverted_index.known. | 60 |
| abstract_inverted_index.member | 45 |
| abstract_inverted_index.model. | 97 |
| abstract_inverted_index.neural | 15, 87, 212 |
| abstract_inverted_index.partly | 26 |
| abstract_inverted_index.reduce | 257 |
| abstract_inverted_index.spinal | 34 |
| abstract_inverted_index.(TRPV1) | 47 |
| abstract_inverted_index.(VT/VF) | 134 |
| abstract_inverted_index.Cardiac | 22 |
| abstract_inverted_index.Chronic | 0 |
| abstract_inverted_index.adverse | 235 |
| abstract_inverted_index.calcium | 170, 178 |
| abstract_inverted_index.cardiac | 78, 112, 121, 236 |
| abstract_inverted_index.chronic | 52, 92 |
| abstract_inverted_index.circuit | 88 |
| abstract_inverted_index.deplete | 77 |
| abstract_inverted_index.fibers, | 80 |
| abstract_inverted_index.induced | 155 |
| abstract_inverted_index.method. | 158 |
| abstract_inverted_index.neurons | 201 |
| abstract_inverted_index.porcine | 96 |
| abstract_inverted_index.propose | 252 |
| abstract_inverted_index.readily | 136 |
| abstract_inverted_index.worsens | 240 |
| abstract_inverted_index.However, | 181 |
| abstract_inverted_index.afferent | 30, 35, 54, 66, 123, 151, 161, 255 |
| abstract_inverted_index.channel. | 48 |
| abstract_inverted_index.chloride | 147 |
| abstract_inverted_index.critical | 14 |
| abstract_inverted_index.depleted | 120 |
| abstract_inverted_index.disrupts | 210 |
| abstract_inverted_index.enhances | 206 |
| abstract_inverted_index.examined | 99 |
| abstract_inverted_index.fibrosis | 184, 233 |
| abstract_inverted_index.function | 24, 208 |
| abstract_inverted_index.ganglion | 200 |
| abstract_inverted_index.handling | 179 |
| abstract_inverted_index.however, | 149 |
| abstract_inverted_index.indicate | 224 |
| abstract_inverted_index.involved | 17 |
| abstract_inverted_index.mapping. | 117 |
| abstract_inverted_index.pathways | 16 |
| abstract_inverted_index.promotes | 68, 232 |
| abstract_inverted_index.receptor | 40 |
| abstract_inverted_index.revealed | 203 |
| abstract_inverted_index.stellate | 199 |
| abstract_inverted_index.subjects | 140 |
| abstract_inverted_index.unstable | 248 |
| abstract_inverted_index.Depleting | 214 |
| abstract_inverted_index.abolished | 126 |
| abstract_inverted_index.afferents | 216 |
| abstract_inverted_index.agonists. | 131 |
| abstract_inverted_index.channels, | 176 |
| abstract_inverted_index.depletion | 152, 162 |
| abstract_inverted_index.dissected | 82 |
| abstract_inverted_index.following | 8, 259 |
| abstract_inverted_index.inducible | 137 |
| abstract_inverted_index.mitigated | 186 |
| abstract_inverted_index.molecular | 104 |
| abstract_inverted_index.potential | 41 |
| abstract_inverted_index.prevented | 153 |
| abstract_inverted_index.proteins. | 180 |
| abstract_inverted_index.reflexes, | 31 |
| abstract_inverted_index.regulated | 27 |
| abstract_inverted_index.responses | 128 |
| abstract_inverted_index.resulting | 245 |
| abstract_inverted_index.signaling | 55 |
| abstract_inverted_index.subfamily | 43 |
| abstract_inverted_index.targeting | 253 |
| abstract_inverted_index.together, | 221 |
| abstract_inverted_index.transient | 39 |
| abstract_inverted_index.Epicardial | 118 |
| abstract_inverted_index.adrenergic | 23, 230 |
| abstract_inverted_index.attenuated | 183 |
| abstract_inverted_index.electrical | 143, 187, 243 |
| abstract_inverted_index.epicardial | 73 |
| abstract_inverted_index.expressing | 37 |
| abstract_inverted_index.expression | 173 |
| abstract_inverted_index.functional | 127 |
| abstract_inverted_index.implicated | 3 |
| abstract_inverted_index.infarction | 10 |
| abstract_inverted_index.integrated | 211 |
| abstract_inverted_index.mechanisms | 102 |
| abstract_inverted_index.myocardial | 9 |
| abstract_inverted_index.normalized | 217 |
| abstract_inverted_index.persistent | 64 |
| abstract_inverted_index.potentials | 168 |
| abstract_inverted_index.processes. | 219 |
| abstract_inverted_index.programmed | 142 |
| abstract_inverted_index.recordings | 196 |
| abstract_inverted_index.transduced | 32 |
| abstract_inverted_index.underlying | 101 |
| abstract_inverted_index.Ventricular | 132 |
| abstract_inverted_index.approaches, | 105 |
| abstract_inverted_index.dysfunction | 231 |
| abstract_inverted_index.instability | 188 |
| abstract_inverted_index.myocardium. | 250 |
| abstract_inverted_index.processing. | 213 |
| abstract_inverted_index.remodeling, | 237 |
| abstract_inverted_index.stimulation | 144 |
| abstract_inverted_index.sympathetic | 29 |
| abstract_inverted_index.transients, | 171 |
| abstract_inverted_index.understood. | 21 |
| abstract_inverted_index.ventricular | 5, 249 |
| abstract_inverted_index.cardioneural | 116 |
| abstract_inverted_index.electrically | 247 |
| abstract_inverted_index.hypothesized | 62 |
| abstract_inverted_index.simultaneous | 115 |
| abstract_inverted_index.cardiomyocyte | 166 |
| abstract_inverted_index.heterogeneity, | 244 |
| abstract_inverted_index.administration; | 148 |
| abstract_inverted_index.resiniferatoxin | 74 |
| abstract_inverted_index.Mechanistically, | 159 |
| abstract_inverted_index.TRPV1-expressing | 79, 254 |
| abstract_inverted_index.afferent-induced | 229 |
| abstract_inverted_index.arrhythmogenesis | 6 |
| abstract_inverted_index.neurotransmission | 67 |
| abstract_inverted_index.electrophysiology, | 113 |
| abstract_inverted_index.sympathoexcitation | 1 |
| abstract_inverted_index.cardiovascular-related | 198 |
| abstract_inverted_index.tachycardia/fibrillation | 133 |
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| cited_by_percentile_year.min | 97 |
| corresponding_author_ids | https://openalex.org/A5080860497 |
| countries_distinct_count | 1 |
| institutions_distinct_count | 11 |
| corresponding_institution_ids | https://openalex.org/I161318765, https://openalex.org/I2800556163, https://openalex.org/I4210146332 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.7300000190734863 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.96668917 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | True |