ArticleNature communications2022
Targeting cardiomyocyte ADAM10 ectodomain shedding promotes survival early after myocardial infarction.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- ADAM and ADAMTS proteases as integrative hubs in heart failure pathogenesis and therapy.iScience · 2026Review
- Chronic inflammation promotes gastric cancer progression via ADAM10-mediated cleavage of CX3CL1.Scientific reports · 2026Article
- NLGN3 contributes to angiogenesis in myocardial infarction via activation of the Gαi1/3-Akt pathway.Basic research in cardiology · 2026Article
- Ion channels and cardiac disease: mechanisms and functions of a disintegrin and metalloproteases and their substrates.Frontiers in cell and developmental biology · 2026Review
- Pathophysiological Roles of the CX3CL1-CX3CR1 Axis in Renal Disease, Cardiovascular Disease, and Cancer.International journal of molecular sciences · 2025Review
- Comparison of the proteomic landscape in experimental ischemia reperfusion with versus without ischemic preconditioning.Scientific reports · 2025Article
- Serum Expression of PDCD4 and ADAM10 in Elderly Patients with Atherosclerotic Acute Myocardial Infarction and Their Combined Predictive Value for Poor Prognosis.Clinical interventions in aging · 2025Article
- ADAM10 Alleviates Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury by Activating the Notch Signaling Pathway.Cell biochemistry and biophysics · 2024Article
- Article
- A methodology to globally assess ectodomain shedding using soluble fractions from the mouse brain.Frontiers in psychiatry · 2024Article
- CX3CL1/CX3CR1 axis alleviates inflammation and apoptosis in human nucleus pulpous cells via M2 macrophage polarization.Experimental and therapeutic medicine · 2023Article
Corrections and comments
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Authors and funding
22 authors at 4 institutions in 1 country.
Funding
Abstract
After myocardial infarction the innate immune response is pivotal in clearing of tissue debris as well as scar formation, but exaggerated cytokine and chemokine secretion with subsequent leukocyte infiltration also leads to further tissue damage. Here, we address the value of targeting a previously unknown a disintegrin and metalloprotease 10 (ADAM10)/CX3CL1 axis in the regulation of neutrophil recruitment early after MI. We show that myocardial ADAM10 is distinctly upregulated in myocardial biopsies from patients with ischemia-driven cardiomyopathy. Intriguingly, upon MI in mice, pharmacological ADAM10 inhibition as well as genetic cardiomycyte-specific ADAM10 deletion improves survival with markedly enhanced heart function and reduced scar size. Mechanistically, abolished ADAM10-mediated CX3CL1 ectodomain shedding leads to diminished IL-1β-dependent inflammation, reduced neutrophil bone marrow egress as well as myocardial tissue infiltration. Thus, our data shows a conceptual insight into how acute MI induces chemotactic signaling via ectodomain shedding in cardiomyocytes.
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Registered trials
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