AP-1 signaling modulates cardiac fibroblast stress responses Article Swipe
Alexander J. Whitehead
,
Hamza Atcha
,
James D. Hocker
,
Bing Ren
,
Adam J. Engler
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1242/jcs.261152
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1242/jcs.261152
Matrix remodeling outcomes largely dictate patient survival post myocardial infarction. Moreover, human-restricted noncoding regulatory elements have been shown to worsen fibrosis, but their mechanism of action remains elusive. Here, we demonstrate, using induced pluripotent stem cell-derived cardiac fibroblasts (iCFs), that inflammatory ligands abundant in the remodeling heart after infarction activate AP-1 transcription factor signaling pathways resulting in fibrotic responses. This observed signaling induces deposition of fibronectin matrix and is further capable of supporting immune cell adhesion; pathway inhibition blocks iCF matrix production and cell adhesion. Polymorphisms in the noncoding regulatory elements within the 9p21 locus (also referred to as ANRIL) redirect stress programs, and in iCFs, they transcriptionally silence the AP-1 inducible transcription factor GATA5. The presence of these polymorphisms modulate iCF matrix production and assembly and reduce cell–cell signaling. These data suggest that this signaling axis is a critical modulator of cardiac disease models and might be influenced by noncoding regulatory elements.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1242/jcs.261152
- https://journals.biologists.com/jcs/article-pdf/136/23/jcs261152/3295428/jcs261152.pdf
- OA Status
- bronze
- Cited By
- 8
- References
- 59
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4388945213
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4388945213Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1242/jcs.261152Digital Object Identifier
- Title
-
AP-1 signaling modulates cardiac fibroblast stress responsesWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2023Year of publication
- Publication date
-
2023-11-23Full publication date if available
- Authors
-
Alexander J. Whitehead, Hamza Atcha, James D. Hocker, Bing Ren, Adam J. EnglerList of authors in order
- Landing page
-
https://doi.org/10.1242/jcs.261152Publisher landing page
- PDF URL
-
https://journals.biologists.com/jcs/article-pdf/136/23/jcs261152/3295428/jcs261152.pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
bronzeOpen access status per OpenAlex
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https://journals.biologists.com/jcs/article-pdf/136/23/jcs261152/3295428/jcs261152.pdfDirect OA link when available
- Concepts
-
Biology, Transcription factor, Cell biology, Fibronectin, Signal transduction, Cell adhesion, Cardiac fibrosis, Cell, Extracellular matrix, Fibrosis, Cancer research, Genetics, Gene, Internal medicine, MedicineTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
8Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 5, 2024: 2, 2023: 1Per-year citation counts (last 5 years)
- References (count)
-
59Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.ANRIL) | 100 |
| abstract_inverted_index.GATA5. | 115 |
| abstract_inverted_index.Matrix | 1 |
| abstract_inverted_index.action | 26 |
| abstract_inverted_index.blocks | 79 |
| abstract_inverted_index.factor | 53, 114 |
| abstract_inverted_index.immune | 74 |
| abstract_inverted_index.matrix | 67, 81, 123 |
| abstract_inverted_index.models | 145 |
| abstract_inverted_index.reduce | 128 |
| abstract_inverted_index.stress | 102 |
| abstract_inverted_index.within | 92 |
| abstract_inverted_index.worsen | 20 |
| abstract_inverted_index.(iCFs), | 39 |
| abstract_inverted_index.capable | 71 |
| abstract_inverted_index.cardiac | 37, 143 |
| abstract_inverted_index.dictate | 5 |
| abstract_inverted_index.disease | 144 |
| abstract_inverted_index.further | 70 |
| abstract_inverted_index.induced | 33 |
| abstract_inverted_index.induces | 63 |
| abstract_inverted_index.largely | 4 |
| abstract_inverted_index.ligands | 42 |
| abstract_inverted_index.pathway | 77 |
| abstract_inverted_index.patient | 6 |
| abstract_inverted_index.remains | 27 |
| abstract_inverted_index.silence | 109 |
| abstract_inverted_index.suggest | 133 |
| abstract_inverted_index.ABSTRACT | 0 |
| abstract_inverted_index.abundant | 43 |
| abstract_inverted_index.activate | 50 |
| abstract_inverted_index.assembly | 126 |
| abstract_inverted_index.critical | 140 |
| abstract_inverted_index.elements | 15, 91 |
| abstract_inverted_index.elusive. | 28 |
| abstract_inverted_index.fibrotic | 58 |
| abstract_inverted_index.modulate | 121 |
| abstract_inverted_index.observed | 61 |
| abstract_inverted_index.outcomes | 3 |
| abstract_inverted_index.pathways | 55 |
| abstract_inverted_index.presence | 117 |
| abstract_inverted_index.redirect | 101 |
| abstract_inverted_index.referred | 97 |
| abstract_inverted_index.survival | 7 |
| abstract_inverted_index.Moreover, | 11 |
| abstract_inverted_index.adhesion. | 85 |
| abstract_inverted_index.adhesion; | 76 |
| abstract_inverted_index.elements. | 153 |
| abstract_inverted_index.fibrosis, | 21 |
| abstract_inverted_index.inducible | 112 |
| abstract_inverted_index.mechanism | 24 |
| abstract_inverted_index.modulator | 141 |
| abstract_inverted_index.noncoding | 13, 89, 151 |
| abstract_inverted_index.programs, | 103 |
| abstract_inverted_index.resulting | 56 |
| abstract_inverted_index.signaling | 54, 62, 136 |
| abstract_inverted_index.deposition | 64 |
| abstract_inverted_index.infarction | 49 |
| abstract_inverted_index.influenced | 149 |
| abstract_inverted_index.inhibition | 78 |
| abstract_inverted_index.myocardial | 9 |
| abstract_inverted_index.production | 82, 124 |
| abstract_inverted_index.regulatory | 14, 90, 152 |
| abstract_inverted_index.remodeling | 2, 46 |
| abstract_inverted_index.responses. | 59 |
| abstract_inverted_index.signaling. | 130 |
| abstract_inverted_index.supporting | 73 |
| abstract_inverted_index.cell–cell | 129 |
| abstract_inverted_index.fibroblasts | 38 |
| abstract_inverted_index.fibronectin | 66 |
| abstract_inverted_index.infarction. | 10 |
| abstract_inverted_index.pluripotent | 34 |
| abstract_inverted_index.cell-derived | 36 |
| abstract_inverted_index.demonstrate, | 31 |
| abstract_inverted_index.inflammatory | 41 |
| abstract_inverted_index.Polymorphisms | 86 |
| abstract_inverted_index.polymorphisms | 120 |
| abstract_inverted_index.transcription | 52, 113 |
| abstract_inverted_index.human-restricted | 12 |
| abstract_inverted_index.transcriptionally | 108 |
| cited_by_percentile_year.max | 99 |
| cited_by_percentile_year.min | 89 |
| countries_distinct_count | 1 |
| institutions_distinct_count | 5 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.7099999785423279 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.89222761 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | True |