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Fibrosis has been shown to develop in individuals with underlying health conditions, especially chronic inflammatory diseases. Fibrosis is often diagnosed in various organs, including the liver, lungs, kidneys, heart, and skin, and has been described as excessive accumulation of extracellular matrix that can affect specific organs in the body or systemically throughout the body. Fibrosis as a chronic condition can result in organ failure and result in death of the individual. Understanding and identification of specific biomarkers associated with fibrosis has emerging potential in the development of diagnosis and targeting treatment modalities. Therefore, in this review, we will discuss multiple signaling pathways such as TGF-β, collagen, angiotensin, and cadherin and outline the chemical nature of the different signaling pathways involved in fibrogenesis as well as the mechanisms. Although it has been well established that TGF-β is the main catalyst initiating and driving multiple pathways for fibrosis, targeting TGF-β can be challenging as this molecule regulates essential functions throughout the body that help to keep the body in homeostasis. We also discuss collagen, angiotensin, and cadherins and their role in fibrosis. We comprehensively discuss the various delivery systems used to target collagen, angiotensin, and cadherins to manage fibrosis. Nevertheless, understanding the steps by which this molecule drives fibrosis development can aid in the development of specific targets of its cascading mechanism. Throughout the review, we will demonstrate the mechanism of fibrosis targeting to improve targeting delivery and therapy.
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http://dx.doi.org/10.1039/d2cc04825f | DOI Listing |
Mech Ageing Dev
August 2025
Department of Cardiology, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, China. Electronic address:
Vascular aging is a critical independent risk factor for cardiovascular disease (CVD), yet its precise molecular mechanisms remain poorly understood. In this study, we generated an ABI3BP knockout mouse to investigate the role of ABI3BP deficiency in angiotensin II (Ang II)-induced vascular aging. The results demonstrated that ABI3BP was highly expressed in AngII-induced senescent vascular smooth muscle cell (VSMC) and vascular tissues, with significantly increased expression also observed in the blood vessels of naturally aged mice.
View Article and Find Full Text PDFJ Bioenerg Biomembr
September 2025
Department of Cardiovascular Medicine, Yan'an People's hospital, No. 16 Qilipu Street, Baota District, Yan'an, 716000, Shaanxi, China.
Myocardial fibrosis (MF) is a key pathological process driving heart failure, characterized by excessive extracellular matrix (ECM) deposition and impaired cardiac function. Although myocyte-specific enhancer factor 2 A (MEF2A) is implicated in cardiac fibroblast activation, its role in MF remains unclear. We manipulated MEF2A expression in cardiac fibroblasts (CFs) through knockdown and overexpression, and assessed fibrosis markers, migration, and RhoA signaling.
View Article and Find Full Text PDFBMC Nephrol
August 2025
Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Background: Alport syndrome (AS) is a hereditary kidney disorder caused by pathogenic variations in COL4 genes and is clinically characterized by hematuria, proteinuria, and progressive renal impairment. IgA nephropathy (IgAN) is a clinicopathological syndrome characterized by the deposition of IgA or IgA-dominant in the glomerular mesangial areas.
Case Presentation: This article reports a case of a 2-year-and-3-month-old female toddler who presented with hematuria and proteinuria.
Inflammation
August 2025
Department of Cardiology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, Jiangxi Province, P.R. China.
Acute kidney injury (AKI) often progresses to chronic kidney disease (CKD), presenting a significant clinical challenge. The renin-angiotensin system (RAS), particularly the protective arm involving Angiotensin-(1-7) (Ang-(1-7)), offers a potential therapeutic target to mitigate this progression. This study explores the effects of Ang-(1-7) in a murine model of ischemia-reperfusion (I/R) injury-induced AKI.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
September 2025
Division of Vascular Surgery, Department of Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States.
Abdominal aortic aneurysm (AAA) is a life-threatening condition with no effective pharmacologic therapies, and increasing evidence suggests that the sympathetic nervous system (SNS) contributes to disease progression. However, the temporal effects of SNS modulation on AAA stability remain unclear. To investigate the impact of SNS modulation on aneurysm outcomes, we induced AAAs in male mice via continuous subcutaneous infusion of angiotensin II.
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