ReviewFrontiers in cell and developmental biology2021
ADAM17, A Key Player of Cardiac Inflammation and Fibrosis in Heart Failure Development During Chronic Catecholamine Stress.
Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Genomic data-driven framework for drug target discovery in atrial fibrillation.Journal of translational medicine · 2025Pooled it
- Murine ADAM15 Deficiency Is Associated With Atrial Remodelling and Atrial Arrhythmia Susceptibility.European journal of clinical investigation · 2026Article
- ADAM17 and its proteolytic targets in disease pathogenesis.The FEBS journal · 2026Review
- ADAM and ADAMTS proteases as integrative hubs in heart failure pathogenesis and therapy.iScience · 2026Review
- Extracellular matrix and proteolysis: mechanisms driving irreversible changes and shaping cell behavior.The FEBS journal · 2026Review
- Article
- Impact of PKC-MAPK Signaling on Cardiac Sympathetic Overactivation in Type-2 Diabetes Mellitus.International journal of molecular sciences · 2026Article
- Dynamic dual regulation of amphiregulin in liver pathophysiology: balancing regeneration and disease progression via the EGFR axis.Frontiers in medicine · 2026Review
- Ion channels and cardiac disease: mechanisms and functions of a disintegrin and metalloproteases and their substrates.Frontiers in cell and developmental biology · 2026Review
- Human single-cell atlas analysis reveals heterogeneous endothelial signaling.bioRxiv : the preprint server for biology · 2025Article
- Exploring Innovative Approaches for Managing Spinal Cord Injury: A Comprehensive Review of Promising Probiotics and Postbiotics.Probiotics and antimicrobial proteins · 2025Review
- JG26 attenuates ADAM17 metalloproteinase-mediated ACE2 receptor processing and SARS-CoV-2 infection in vitro.Pharmacological reports : PR · 2025Article
- Article
- Triglyceride glucose index: a significant prognostic marker of heart failure in patients with chronic kidney disease.Renal failure · 2024Article
- GPER-1 Rapid Regulation Influences p-Akt Expression to Resist Stress-Induced Injuries in a Sex-Specific Manner.Physiological research · 2024Article
- Development of a small animal model replicating core characteristics of takotsubo syndrome in humans.European heart journal open · 2024Article
- Article
- CP-25 inhibits the hyperactivation of rheumatic synoviocytes by suppressing the switch in GCell communication and signaling : CCS · 2023Article
- Carbon dioxide and MAPK signalling: towards therapy for inflammation.Cell communication and signaling : CCS · 2023Review
- Estradiol mitigates stress-induced cardiac injury and inflammation by downregulating ADAM17 via the GPER-1/PI3K signaling pathway.Cellular and molecular life sciences : CMLS · 2023Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure development is characterized by persistent inflammation and progressive fibrosis owing to chronic catecholamine stress. In a chronic stress state, elevated catecholamines result in the overstimulation of beta-adrenergic receptors (βARs), specifically β2-AR coupling with Gαi protein. Gαi signaling increases the activation of receptor-stimulated p38 mitogen-activated-protein-kinases (p38 MAPKs) and extracellular signal-regulated kinases (ERKs). Phosphorylation by these kinases is a common way to positively regulate the catalytic activity of A Disintegrin and Metalloprotease 17 (ADAM17), a metalloprotease that has grown much attention in recent years and has emerged as a chief regulatory hub in inflammation, fibrosis, and immunity due to its vital proteolytic activity. ADAM17 cleaves and activates proinflammatory cytokines and fibrotic factors that enhance cardiac dysfunction via inflammation and fibrosis. However, there is limited information on the cardiovascular aspect of ADAM17, especially in heart failure. Hence, this concise review provides a comprehensive insight into the structure of ADAM17, how it is activated and regulated during chronic catecholamine stress in heart failure development. This review highlights the inflammatory and fibrotic roles of ADAM17's substrates; Tumor Necrosis Factor α (TNFα), soluble interleukin-6 receptor (sIL-6R), and amphiregulin (AREG). Finally, how ADAM17-induced chronic inflammation and progressive fibrosis aggravate cardiac dysfunction is discussed.
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Registered trials
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