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Non-alcoholic fatty liver disease (NAFLD) figures prominently into the clinical hepatology landscape. NAFLD represents a disease spectrum comprising simple steatosis, steatosis with elevated liver enzymes, and non-alcoholic steatohepatitis (NASH), the entity with clear potential for fibrosis progression. Risk factors associated with fibrosis progression in NASH include histologic findings of lobular inflammation and any fibrosis as well as clinical comorbidities that include type 2 diabetes, obesity, and metabolic syndrome. Liver biopsy remains the gold standard in evaluating NASH; however, noninvasive methods are accumulating evidence for a growing role in identifying patients at increased risk to develop NASH, fibrosis, and potentially cirrhosis.
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http://dx.doi.org/10.1016/j.gtc.2019.09.002 | DOI Listing |
Sci Transl Med
September 2025
Department of Medicine, Columbia University Irving Medical Center, New York, NY 10032, USA.
Hepatocyte apoptosis is a key feature of metabolic dysfunction-associated steatohepatitis (MASH), but the fate of apoptotic hepatocytes in MASH is poorly understood. Here, we explore the hypotheses that clearance of dead hepatocytes by liver macrophages (efferocytosis) is impaired in MASH because of low expression of the efferocytosis receptor T cell immunoglobulin and mucin domain containing 4 (TIM4; gene ) by MASH liver macrophages, which then drives liver fibrosis in MASH. We show that apoptotic hepatocytes accumulate in human and experimental MASH, using mice fed the fructose-palmitate-cholesterol (FPC) diet or the high-fat, choline-deficient amino acid-defined (HF-CDAA) diet.
View Article and Find Full Text PDFMol Cell Biochem
September 2025
Peking University Third Hospital, Beijing, China.
Cardiovascular-Kidney-Metabolic (CKM) syndrome, a newly defined systemic disorder, is characterized by the pathological interplay among diabetes, chronic kidney disease (CKD), and cardiovascular disease (CVD). Recent studies have identified chronic inflammation not only as a central mediator in the pathological progression of CKM syndrome but also as a pivotal molecular hub that drives coordinated damage across multiple organ systems. Mechanistic investigations have revealed that aberrant activation of signaling pathways such as NF-κB, Wnt, PI3K-AKT, JAK-STAT, and PPAR constitutes a complex inflammatory regulatory network.
View Article and Find Full Text PDFMol Cell Biol
September 2025
Medical School of Tianjin University, Tianjin, China.
Over the past few decades, liver disease has emerged as one of the leading causes of death worldwide. Liver injury is frequently associated with infections, alcohol consumption, or obesity, which trigger hepatic inflammation and ultimately lead to progressive fibrosis and carcinoma. Although various cell populations contribute to inflammatory and fibrogenic processes in the liver, macrophages serve as a pivotal mediator.
View Article and Find Full Text PDFHead Neck
September 2025
Department of Head and Neck Surgery, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA.
Background: Late radiation-associated dysphagia (late-RAD) commonly presents in patients with signs of hypoglossal neuropathy, with hallmark clinical features including lingual atrophy, deviation, and fasciculation. Gold-standard electromyography (EMG) has not been used to explore the frequency of hypoglossal neuropathy in patients with late-RAD.
Methods: Exploratory post hoc secondary analysis of MANTLE trial (NCT03612531) was completed.
Clin Kidney J
September 2025
Department of Nephrology. University Clinical Hospital, INCLIVA, Valencia. RICORS Renal Instituto de salud Carlos III, Valencia. Spain.
Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a major contributor to systemic metabolic dysfunction and is increasingly recognized as a risk enhancer for both cardiovascular disease (CVD) and chronic kidney disease (CKD). This review explores the complex interconnections between MASLD, CVD, and CKD, with emphasis on shared pathophysiological mechanisms and the clinical implications for risk assessment and management. We describe the crosstalk among the liver, heart, and kidneys, focusing on insulin resistance, chronic inflammation, and progressive fibrosis as key mediators.
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