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Valsartan is an orally active non-peptide angiotensin receptor antagonist, an effective and well-tolerated anti-hypertensive drug. Besides its antihypertensive action, it has clinical implications in many other disorders, like heart failure (HF), arrhythmia, chronic kidney disease (CKD), diabetic complications (DM), atherosclerosis, etc. Besides angiotensin receptor blocking activity, valsartan reduces circulating levels of biochemical markers, such as hs-CRP, which is responsible for its anti-inflammatory and anti-oxidant activity. Moreover, valsartan also acts by inhibiting or inducing various signalling pathways, such as inducing autophagy the AKT/mTOR/S6K pathway or inhibiting the TLR/NF-kB pathway. The current review exhaustively discusses the therapeutic implications of valsartan with specific emphasis on the mechanism of action in various disorders. The article provides a detailed spectrum of the therapeutic profile of valsartan and will likely be very useful to researchers working in the relevant research areas.
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http://dx.doi.org/10.2174/2589977515666230717120828 | DOI Listing |
Nanoscale
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 PDFLiver Int
October 2025
GastroZentrum Hirslanden, Digestive Disease Center, Zürich, Switzerland.
Background And Aims: Cholangiopathies, including primary sclerosing cholangitis (PSC), primary biliary cholangitis (PBC), and post-COVID-19 cholangiopathy (PCC), involve chronic cholangiocyte injury, senescence, epithelial-stromal crosstalk, and progressive fibrosis. However, effective in vitro models to capture these interactions are limited. Here, we present a scaffold-free 3D multilineage spheroid model, composed of hepatocyte-like cells (HepG2), cholangiocytes (H69), and hepatic stellate cells (LX-2), designed to recapitulate early fibrogenic responses driven by senescent cholangiocytes.
View Article and Find Full Text PDFAnn Palliat Med
September 2025
Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Radical esophagectomy remains the cornerstone of curative treatment for esophageal cancer, but is frequently complicated by postoperative events, most notably anastomotic leakage. Anastomotic leakage, occurring in up to 30% of cases, is multifactorial in origin and significantly increases morbidity and mortality. This review aims to summarize current management strategies, highlight emerging therapies, and identify persistent clinical challenges related to this complication.
View Article and Find Full Text PDFNeuroinflammation has emerged as a central and dynamic component of the pathophysiology underlying a wide range of neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and multiple sclerosis. Far from being a secondary consequence of neuronal damage, inflammatory processes (mediated by microglia, astrocytes, peripheral immune cells, and associated molecular mediators) actively shape disease onset, progression, and symptomatology. This review synthesizes current knowledge on the cellular and molecular mechanisms that govern neuroinflammatory responses, emphasizing both shared and disease-specific pathways.
View Article and Find Full Text PDFNature
September 2025
Centre for Evolution and Cancer, Institute of Cancer Research, London, UK.
Cancer development and response to treatment are evolutionary processes, but characterizing evolutionary dynamics at a clinically meaningful scale has remained challenging. Here we develop a new methodology called EVOFLUx, based on natural DNA methylation barcodes fluctuating over time, that quantitatively infers evolutionary dynamics using only a bulk tumour methylation profile as input. We apply EVOFLUx to 1,976 well-characterized lymphoid cancer samples spanning a broad spectrum of diseases and show that initial tumour growth rate, malignancy age and epimutation rates vary by orders of magnitude across disease types.
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