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Background: Fibrosis is a pathological complication that arises from an abnormal tissue healing response to chronic inflammation or repeated injury. It is characterized by Excessive Extracellular Matrix (ECM) deposition, leading to progressive organ dysfunction. Chronic Kidney Disease of unknown etiology (CKDu) is a newly recognized public health crisis characterized by slow, irreversible progression and late-stage asymptomatic onset.
Objectives: To identify and analyze therapeutic targets, experimental strategies, and emerging treatments for renal fibrosis, with a focus on CKDu.
Methods: Experimental data on potential therapeutic targets, including - - and were compiled and analyzed. Specific attention was given to the roles of and in fibrosis. Data on phytopharmaceuticals, such as and , as well as emerging treatments like were gathered and reviewed.
Results: Therapeutic targets address key molecular pathways involved in fibrogenesis, including chemokine signaling (CCR1, CCR2, and CCL2), pro-fibrotic mediators (TGF-β and CTGF), and oxidative stress (Nox1/4). Phytopharmaceuticals, such as and bio-fibrin, demonstrated antifibrotic potential through their anti-inflammatory and ECM-modulating effects. Preclinical studies on stem cell therapies highlighted regenerative benefits in managing renal fibrosis. Experimental data on Cx43 and DDR1 supported their role in fibrotic progression and potential as therapeutic targets.
Conclusion: The study provides a comprehensive analysis of antifibrotic strategies, including validated molecular targets, phytopharmaceuticals, and innovative therapies like stem cell treatments. These findings underscore the need for focused research and development of effective interventions for CKDu and related fibrotic diseases.
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http://dx.doi.org/10.2174/0118715303374764250612052832 | DOI Listing |
Haematologica
September 2025
Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD,.
Immunotherapies, including cell therapies, are effective anti-cancer agents. However, cellular product persistence can be limiting with short functional duration of activity contributing to disease relapse. A variety of manufacturing protocols are used to generate therapeutic engineered T-cells; these differ in techniques used for T-cell isolation, activation, genetic modification, and other methodology.
View Article and Find Full Text PDFMol Cancer Ther
September 2025
Case Western Reserve University School of Medicine, Cleveland, OH, United States.
The estrogen receptor (ER or ERα) remains the primary therapeutic target for luminal breast cancer, with current treatments centered on competitive antagonists, receptor down-regulators, and aromatase inhibitors. Despite these options, resistance frequently emerges, highlighting the need for alternative targeting strategies. We discovered a novel mechanism of ER inhibition that targets the previously unexplored interface between the DNA-binding domain (DBD) and ligand-binding domain (LBD) of the receptor.
View Article and Find Full Text PDFNanoscale
September 2025
Institute of Health Innovation & Technology, National University of Singapore, Singapore, 117599, Singapore.
The rapid increase in multidrug-resistant (MDR) bacteria and biofilm-associated infections has intensified the global need for innovative antimicrobial strategies. Phage therapy offers promising precision against MDR pathogens by utilizing the natural ability of phages to specifically infect and lyse bacteria. However, their clinical application is hampered by challenges such as narrow host range, immune clearance and limited efficacy within biofilms.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
September 2025
Vascular Biology Program, Boston Children's Hospital and Harvard Medical School, MA (K. Cui, B.Z., B.W., S.E.-B., A.V., H.C.).
Background: Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipid-laden foam cells and plaques within the arterial wall. Dysfunctional vascular smooth muscle cells (VSMCs), fibroblasts, endothelial cells, and macrophages contribute to disease progression. Here, we report that macrophage-specific expression of epsins, highly conserved endocytic adaptor proteins involved in clathrin-mediated endocytosis, accelerates atherosclerosis in Western diet-fed mice.
View Article and Find Full Text PDFFuture Oncol
September 2025
Department of General Surgery, Institute of General Surgery, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou University, Yangzhou, China.
Immune checkpoint therapy has demonstrated significant potential in the treatment of various solid tumors. Among these, tumor-induced immunosuppression mediated by programmed cell death protein 1 (PD-1) represents a critical checkpoint. PD-1/programmed death-ligand 1 (PD-L1) inhibitors have been proven to exhibit substantial efficacy in solid tumors such as melanoma and bladder cancer.
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