ReviewActa pharmacologica Sinica2015
The emerging roles of β-arrestins in fibrotic diseases.
Review in Acta pharmacologica Sinica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Neuroinflammation and noradrenergic modulation with β2-adrenoceptors: Emerging therapeutic targets for Parkinson's diseases.Neural regeneration research · 2026Article
- Agonist-specific conformational dynamics at the βBritish journal of pharmacology · 2026Article
- Mechanical mechanics-reclaiming a new battlefield for chronic liver disease.Journal of advanced research · 2026Review
- Biased Orthosteric Agonism and Allosteric Modulation: Emerging Strategies for Developing New Class of β-Agonists for Obstructive Airway Diseases.American journal of respiratory cell and molecular biology · 2025Review
- β-arrestin2: an emerging player and potential therapeutic target in inflammatory immune diseases.Acta pharmacologica Sinica · 2025Review
- Major pathophysiological changes in pulmonary disease provided a molecular insight based on deep learning approach.Scientific reports · 2025Article
- G protein-coupled receptor-mediated renal fibrosis: a key focus on kidney disease drug development.Frontiers in pharmacology · 2025Review
- Application of RNA-Seq Technology for Screening Reproduction-Related Differentially Expressed Genes in Tibetan and Yorkshire Pig Ovarian Tissue.Veterinary sciences · 2024Article
- β-Arrestin pathway activation by selective ATR1 agonism promotes calcium influx in podocytes, leading to glomerular damage.Clinical science (London, England : 1979) · 2023Article
- β-Blockers in Hepatosplenic Schistosomiasis: A Narrative Review.The American journal of tropical medicine and hygiene · 2023Review
- Hepatic β-arrestins: potential roles in liver health and disease.Molecular biology reports · 2023Review
- FGF9 Recruits β-Catenin to Increase Hepatic ECM Synthesis and Promote NASH-Driven HCC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- β-arrestin2 deficiency ameliorates S-100-induced autoimmune hepatitis in mice by inhibiting infiltration of monocyte-derived macrophage and attenuating hepatocyte apoptosis.Acta pharmacologica Sinica · 2023Article
- GPR35 acts a dual role and therapeutic target in inflammation.Frontiers in immunology · 2023Review
- Lysyl oxidase promotes renal fibrosis via accelerating collagen cross-link driving by β-arrestin/ERK/STAT3 pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Beta-blockers in patients with liver cirrhosis: Pragmatism or perfection?Frontiers in medicine · 2022Review
- Research Progress of Fibroblast Growth Factor 21 in Fibrotic Diseases.Oxidative medicine and cellular longevity · 2022Review
- Targeting GPCRs to treat cardiac fibrosis.Frontiers in cardiovascular medicine · 2022Review
- β-Arrestin2 deficiency attenuates oxidative stress in mouse hepatic fibrosis through modulation of NOX4.Acta pharmacologica Sinica · 2021Article
- Sodium butyrate protects against lipopolysaccharide-induced liver injury partially via the GPR43/ β-arrestin-2/NF-κB network.Gastroenterology report · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β-Arrestins and β-arrestin2 are important adaptor proteins and signal transduction proteins that are mainly involved in the desensitization and internalization of G-protein-coupled receptors. Fibrosis is characterized by accumulation of excess extracellular matrix (ECM) molecules caused by chronic tissue injury. If highly progressive, the fibrotic process leads to organ malfunction and, eventually, death. The incurable lung fibrosis, renal fibrosis and liver fibrosis are among the most common fibrotic diseases. Recent studies show that β-arrestins can activate signaling cascades independent of G-protein activation and scaffold many intracellular signaling networks by diverse types of signaling pathways, including the Hedgehog, Wnt, Notch and transforming growth factor-β pathways, as well as downstream kinases such as MAPK and PI3K. These signaling pathways are involved in the pathological process of fibrosis and fibrotic diseases. This β-arrestin-mediated regulation not only affects cell growth and apoptosis, but also the deposition of ECM, activation of inflammatory response and development of fibrotic diseases. In this review, we survey the involvement of β-arrestins in various signaling pathways and highlight different aspects of their regulation of fibrosis. We also discuss the important roles of β-arrestins in the process of fibrotic diseases by regulating the inflammation and deposit of ECM. It is becoming more evident that targeting β-arrestins may offer therapeutic potential for the treatment of fibrotic diseases.
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