Increased Risk of Cancer—An Integral Component of the Cardio–Renal–Metabolic Disease Cluster and Its Management DOI Creative Commons
Eberhard Standl, Oliver Schnell

Cells, Год журнала: 2025, Номер 14(8), С. 564 - 564

Опубликована: Апрель 9, 2025

Cancer risk increases by 25 to 250% not only in dysmetabolic obese or overweight people with overt type 2 diabetes but also individuals intermediate hyperglycemia (pre-diabetes), especially pronounced of pancreatic hepatocellular cancer and obesity-related cancers, e.g., colorectal kidney bladder men, endometrial breast cancers women. may often be present before upon the diagnosis diabetes, as there is a common pathogenetic dysmetabolic–inflammatory background insulin resistance for developing cardiorenal disease, parallel. The mechanisms involved relate hyperinsulinemia potential carcinogenic priming event ectopic visceral, hepatic, pancreatic, renal fat accumulation that subsequently fuel inflammation lipo-oncogenic signals, causing mitochondrial oxidative stress deregulation. Moreover, foster mitogenic MAP kinase-related signaling, which can occur via IGF1 receptors due increased free levels obesity. Weight reduction 10% more pre-diabetes, through intensive lifestyle intervention bariatric (=metabolic) surgery treatment GLP-1 receptor agonists metformin, associated significantly lower incidence “diabesity”-associated cancers. In conclusion, seems huge utility adopting new “Cardio-Renal-Metabolic-Cancer Syndrome” approach, looking at time addition proactively screening undiagnosed dysglycemia.

Язык: Английский

Expanding Indications in Transplant Oncology DOI Open Access

Erlind Allkushi,

Chase J. Wehrle, JaeKeun Kim

и другие.

Cancers, Год журнала: 2025, Номер 17(5), С. 773 - 773

Опубликована: Фев. 25, 2025

Liver transplantation is aptly described as the only curative treatment for cirrhosis and with co-morbid hepatocellular carcinoma (HCC). Its utility in management of various other primary secondary liver cancers gaining traction rapidly, more thorough assessments on broader populations continuing to emerge. Most prominently, this includes colorectal cancer metastasis (CRLM), cholangiocarcinoma (CCA), neuroendocrine tumors (NETs), more. Furthermore, despite being a well HCC many years, growing evidence supports change oncological strategy HCC, broadened selection criteria advanced systemic locoregional therapies available. Our review aims describe supporting expansion indications oncologic tumors.

Язык: Английский

Процитировано

0
Fat, fibrosis, and the future: navigating the maze of MASLD/MASH DOI Creative Commons
Scott L. Friedman

Journal of Clinical Investigation, Год журнала: 2025, Номер 135(7)

Опубликована: Март 31, 2025

Язык: Английский

Процитировано

0
Cardiovascular-liver-metabolic health: Time to integrate liver assessment into cardiology practice? DOI

Luan C V Lima,

Lubna Al‐Sharif, Matheus Souza

и другие.

Trends in Cardiovascular Medicine, Год журнала: 2025, Номер unknown

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0
Genomics-Informed Drug Repurposing Strategy Identifies Novel Therapeutic Targets for Metabolic Dysfunction-Associated Steatotic Liver Disease. DOI Creative Commons
Hannah M. Seagle,

Alexis T. Akerele,

Joseph A. DeCorte

и другие.

medRxiv (Cold Spring Harbor Laboratory), Год журнала: 2025, Номер unknown

Опубликована: Фев. 21, 2025

Summary Identification of drug-repurposing targets with genetic and biological support is an economically temporally efficient strategy for improving treatment diseases. We employed a cross-disciplinary approach to identify potential treatments metabolic dysfunction associated steatotic liver disease (MASLD) using humans as model organism. identified 212 putative causal genes MASLD data from large multi-ancestry association study, which 158 (74.5%) are novel. From this set we 57 that encode druggable protein targets, where the effects increasing genetically predicted gene expression on risk align function drug target. These were then evaluated evidence efficacy Mendelian randomization, pathway analysis, structural modeling. Using these approaches, present compelling suggest activation FADS1 by icosopent ethyl well S1PR2 fingolimod could be promising therapeutic strategies MASLD.

Язык: Английский

Процитировано

0
MASLD: Prevalence, Mechanisms, and Sex-Based Therapies in Postmenopausal Women DOI Creative Commons
Ilaria Milani,

Marianna Chinucci,

Frida Leonetti

и другие.

Biomedicines, Год журнала: 2025, Номер 13(4), С. 855 - 855

Опубликована: Апрель 2, 2025

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic influenced by genetic, lifestyle, and environmental factors. While MASLD more prevalent in men, women are at increased risk after menopause, highlighting critical pathogenetic role of sex hormones. The complex interplay between estrogen deficiency, visceral fat accumulation, metabolic syndrome (MetS), inflammation accelerates progression, increases cardiovascular (CV) risk, triggers a cycle worsening adiposity, dysfunction, psychological problems, including eating disorders. Weight loss postmenopausal can significantly improve both outcomes, helping to prevent related conditions. This review examines prevalence MASLD, its comorbidities (type 2 diabetes T2D, CV, mental disorders), mechanisms, pharmacological treatment with GLP-1 receptor agonists (GLP1-RAs), focus on women. Given use GLP1-RAs obesity T2D patients, increase MetS this analyzes potential stable GLP-1–estrogen conjugate as therapeutic approach subgroup. By combining synergistic effects hormones, dual agonist has been shown food intake reward suppression, resulting greater weight improved insulin sensitivity, glucose, lipid metabolism. Therefore, we hypothesize that pharmacotherapy may provide targeted benefits than either hormone alone protecting liver, β-cells, overall health. As these only supported preclinical data, highlights need for future research evaluate confirm mechanisms efficacy clinical settings, particularly

Язык: Английский

Процитировано

0
Overcoming Barriers to Unlock the Therapeutic Potential of Saroglitazar for the Management of Metabolic Dysfunction-Associated Steatotic Liver Disease DOI

Murali Krishna Moka,

Deepalaxmi Rathakrishnan,

D K Sriram

и другие.

Clinical Nutrition, Год журнала: 2025, Номер 49, С. 52 - 56

Опубликована: Апрель 5, 2025

Язык: Английский

Процитировано

0
Type I IFN receptor blockade alleviates liver fibrosis through macrophage-derived STAT3 signaling DOI Creative Commons

Soo-Jeung Park,

Josefina Garcia Diaz,

Tina Comlekoglu

и другие.

Frontiers in Immunology, Год журнала: 2025, Номер 16

Опубликована: Апрель 7, 2025

Liver macrophages play a role in the development of liver fibrosis progression via regulation inflammatory signaling. However, precise mechanisms contributing to remain unclear. Using preclinical model CCl4-treated mice, we determined composition immune cells and alteration gene expression. Our findings revealed significant increase macrophages, particularly those derived from infiltrating blood monocytes, fibrotic mice. Moreover, expression levels type I IFN signature genes such as IFNα , IFNβ ISG15 USP18 Ifi44 Ifit1 Ifit2 IRF3 IRF7 were elevated To determine signaling fibrosis, administered an IFNAR-1 antibody block this pathway for 3 days prior harvesting liver. Notably, blockade reduced macrophage numbers compared control mice alleviated with increased hepatocyte proliferation apoptosis. The ratio P-STAT3/P-STAT1 monocyte-derived was group related appearance M2 differentiation. Additionally, single-cell RNA-seq analysis indicated that IFNAR affected pathways involved regeneration prevention. Taken together, alleviates by modulating responses. These results provide insights developing anti-fibrotic therapies against

Язык: Английский

Процитировано

0
Increased Risk of Cancer—An Integral Component of the Cardio–Renal–Metabolic Disease Cluster and Its Management DOI Creative Commons
Eberhard Standl, Oliver Schnell

Cells, Год журнала: 2025, Номер 14(8), С. 564 - 564

Опубликована: Апрель 9, 2025

Cancer risk increases by 25 to 250% not only in dysmetabolic obese or overweight people with overt type 2 diabetes but also individuals intermediate hyperglycemia (pre-diabetes), especially pronounced of pancreatic hepatocellular cancer and obesity-related cancers, e.g., colorectal kidney bladder men, endometrial breast cancers women. may often be present before upon the diagnosis diabetes, as there is a common pathogenetic dysmetabolic–inflammatory background insulin resistance for developing cardiorenal disease, parallel. The mechanisms involved relate hyperinsulinemia potential carcinogenic priming event ectopic visceral, hepatic, pancreatic, renal fat accumulation that subsequently fuel inflammation lipo-oncogenic signals, causing mitochondrial oxidative stress deregulation. Moreover, foster mitogenic MAP kinase-related signaling, which can occur via IGF1 receptors due increased free levels obesity. Weight reduction 10% more pre-diabetes, through intensive lifestyle intervention bariatric (=metabolic) surgery treatment GLP-1 receptor agonists metformin, associated significantly lower incidence “diabesity”-associated cancers. In conclusion, seems huge utility adopting new “Cardio-Renal-Metabolic-Cancer Syndrome” approach, looking at time addition proactively screening undiagnosed dysglycemia.

Язык: Английский

Процитировано

0