Publications by authors named "Jose Carlos Fernandez-Checa"
Article Synopsis
- Inclusion body myositis (IBM) is a rare inflammatory muscle disease causing muscle weakness and is characterized by specific abnormalities in muscle tissue, but understanding of its causes and treatments is limited due to the lack of effective disease models.
- In a study comparing fibroblast samples from IBM patients and healthy individuals, researchers identified 778 genes with significant differences in expression, particularly related to inflammation and mitochondrial functions, highlighting an increased inflammatory response in IBM cells.
- The findings revealed key mitochondrial dysfunctions, including decreased genetic material, impaired respiration, and increased oxidative stress, suggesting that inflammation and oxidative stress could serve as potential indicators for disease progression in IBM patients.
Background And Aims: Janus kinase 2 (JAK2) signaling is increased in human and experimental liver fibrosis with portal hypertension. JAK2 inhibitors, such as pacritinib, are already in advanced clinical development for other indications and might also be effective in liver fibrosis. Here, we investigated the antifibrotic role of the JAK2 inhibitor pacritinib on activated hepatic stellate cells (HSCs) in vitro and in two animal models of liver fibrosis in vivo .
View Article and Find Full Text PDFDisrupted Mitochondrial and Metabolic Plasticity Underlie Comorbidity between Age-Related and Degenerative Disorders as Parkinson Disease and Type 2 Diabetes Mellitus.
Antioxidants (Basel)
October 2020
Idiopathic Parkinson's disease (iPD) and type 2 diabetes mellitus (T2DM) are chronic, multisystemic, and degenerative diseases associated with aging, with eventual epidemiological co-morbidity and overlap in molecular basis. This study aims to explore if metabolic and mitochondrial alterations underlie the previously reported epidemiologic and clinical co-morbidity from a molecular level. To evaluate the adaptation of iPD to a simulated pre-diabetogenic state, we exposed primary cultured fibroblasts from iPD patients and controls to standard (5 mM) and high (25 mM) glucose concentrations to further characterize metabolic and mitochondrial resilience.
View Article and Find Full Text PDFPRKN encodes an E3-ubiquitin-ligase involved in multiple cell processes including mitochondrial homeostasis and autophagy. Previous studies reported alterations of mitochondrial function in fibroblasts from patients with PRKN mutation-associated Parkinson's disease (PRKN-PD) but have been only conducted in glycolytic conditions, potentially masking mitochondrial alterations. Additionally, autophagy flux studies in this cell model are missing.
View Article and Find Full Text PDFArticle Synopsis
- GDF11 is identified as a crucial factor in regulating cell differentiation and has been poorly studied in cancer, especially in hepatocellular carcinoma (HCC), an aggressive liver cancer.
- Treatment with GDF11 reduced the proliferation and colony forming ability of HCC cell lines, altering key cell cycle proteins and indicating compromised cell functionality.
- Additionally, GDF11 treatment led to long-lasting effects on self-renewal capacity and significantly reduced cell migration and proliferation in vivo, suggesting its potential as a tumor suppressor in HCC.
Aim: Zinc has proved its efficacy in many models of ischemia reperfusion (I/R) injury. In this study, we used zinc acexamate (ZAC) as an exogenous source of zinc against renal I/R injury and we investigated whether its protective effects are mediated by the decrease of oxidative stress, inflammation, and mitochondria induced-apoptosis.
Methods: Rats were orally pretreated with vehicle or ZAC (10 or 100 mg/kg) 24 h and 30 min prior to 1 h of bilateral renal warm ischemia and 2 h of reperfusion.