ArticleScientific reports2017
Cathepsin D regulates lipid metabolism in murine steatohepatitis.
Article in Scientific reports, 2017. 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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Who cites it
33 citing papers in PubMed, 74 citations in OpenAlex.
- Cathepsin D-driven IL2RG-JAK2 signal hijacking disrupts hepatic insulin action: mechanism-grounded proof that targeting cathepsin D prevents prediabetes.International journal of obesity (2005) · 2026Article
- Plasma-targeted proteomic and lipidomic profiling of MASLD, MASH, and hepatitis C virus infection.Clinical proteomics · 2026Article
- Folic Acid Targeting Shared Sepsis-Osteoporosis Pathogenesis: From Computational Discovery to Dynamic Binding Mechanisms.ACS omega · 2026Article
- Optimization of protein extraction and digestion workflows for proteomic analysis of saliva, salivary stones and kidney stones.Frontiers in molecular biosciences · 2026Article
- A human-mouse atlas of intrarenal myeloid cells identifies conserved disease-associated macrophages in lupus nephritis.The Journal of experimental medicine · 2025Article
- Cathepsins: Emerging targets in the tumor ecosystem to overcome cancers.Seminars in cancer biology · 2025Review
- Inhibition of intracellular versus extracellular cathepsin D differentially alters the liver lipidome of mice with metabolic dysfunction-associated steatohepatitis.The FEBS journal · 2025Article
- Associations of cathepsins with pulmonary arterial hypertension mediated by circulating metabolites: A Mendelian randomization study.Medicine · 2025Article
- Physiological Responses to Acute Heat Stress in Rohu, Labeo rohita: Insights from Liver Proteomics.Marine biotechnology (New York, N.Y.) · 2024Article
- Myosteatosis: Diagnosis, pathophysiology and consequences in metabolic dysfunction-associated steatotic liver disease.JHEP reports : innovation in hepatology · 2024Review
- Proteomic analysis of sialoliths from calcified, lipid and mixed groups as a source of potential biomarkers of deposit formation in the salivary glands.Clinical proteomics · 2023Article
- Molecular programming modulates hepatic lipid metabolism and adult metabolic risk in the offspring of obese mothers in a sex-specific manner.Communications biology · 2022Article
- All Roads Lead to Cathepsins: The Role of Cathepsins in Non-Alcoholic Steatohepatitis-Induced Hepatocellular Carcinoma.Biomedicines · 2022Review
- Restoration of Cathepsin D Level via L-Serine Attenuates PPA-Induced Lysosomal Dysfunction in Neuronal Cells.International journal of molecular sciences · 2022Article
- A Transcriptomic Response toInternational journal of molecular sciences · 2022Article
- Cathepsin D as a potential therapeutic target to enhance anticancer drug-induced apoptosis via RNF183-mediated destabilization of Bcl-xL in cancer cells.Cell death & disease · 2022Article
- Identifying Autophagy-Related lncRNAs and Potential ceRNA Networks in NAFLD.Frontiers in genetics · 2022Article
- Identification of monocyte-associated genes as predictive biomarkers of heart failure after acute myocardial infarction.BMC medical genomics · 2021Article
- Autophagy in liver diseases.World journal of hepatology · 2021Review
- Precision N-Glycoproteomic Profiling of Murine Peritoneal Macrophages After Different Stimulations.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Due to the obesity epidemic, non-alcoholic steatohepatitis (NASH) is a prevalent liver disease, characterized by fat accumulation and inflammation of the liver. However, due to a lack of mechanistic insight, diagnostic and therapeutic options for NASH are poor. Recent evidence has indicated cathepsin D (CTSD), a lysosomal enzyme, as a marker for NASH. Here, we investigated the function of CTSD in NASH by using an in vivo and in vitro model. In addition to diminished hepatic inflammation, inhibition of CTSD activity dramatically improved lipid metabolism, as demonstrated by decreased plasma and liver levels of both cholesterol and triglycerides. Mechanistically, CTSD inhibition resulted in an increased conversion of cholesterol into bile acids and an elevated excretion of bile acids via the feces, indicating that CTSD influences lipid metabolism. Consistent with these findings, treating Wt BMDMs with PepA in vitro showed a similar decrease in inflammation and an analogous effect on cholesterol metabolism.
conclusionCTSD is a key player in the development of hepatic inflammation and dyslipidemia. Therefore, aiming at the inhibition of the activity of CTSD may lead to novel treatments to combat NASH.
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