Publications by authors named "Yohei Fushimura"
Purpose: To determine the predictors of wound recurrence after complete wound healing in patients with chronic limb-threatening ischemia (CLTI) who underwent endovascular therapy (EVT) for infrapopliteal (IP) lesions with consideration of IP arterial anatomic severity, including classification by the Global Limb Anatomic Staging System (GLASS).
Materials And Methods: This retrospective single-center study assessed patients with de novo CLTI limbs with tissue loss treated via EVT for IP lesions from September 2016 to May 2021. Among these patients, 149 consecutive limbs from 133 patients who achieved complete wound healing were enrolled.
Background: To investigate the prognostic impact of femoropopliteal (FP) arterial anatomic severity including classification by the global limb anatomic staging system (GLASS) on wound healing in patients with chronic limb-threatening ischemia (CLTI) who had undergone endovascular therapy (EVT) only for FP lesions.
Methods: This was a retrospective single-center study. We treated 349 consecutive de novo CLTI limbs with tissue loss from January 2017 to May 2021.
Orotic acid protects pancreatic β cell by p53 inactivation in diabetic mouse model.
Biochem Biophys Res Commun
December 2021
Impairment of pancreatic β cells is a principal driver of the development of diabetes. Restoring normal insulin release from the β cells depends on the ATP produced by the intracellular mitochondria. In maintaining mitochondrial function, the tumor suppressor p53 has emerged as a novel regulator of metabolic homeostasis and participates in adaptations to nutritional changes.
View Article and Find Full Text PDFTIGAR reduces smooth muscle cell autophagy to prevent pulmonary hypertension.
Am J Physiol Heart Circ Physiol
November 2020
Article Synopsis
- TIGAR is a protein that inhibits autophagy and reactive oxygen species (ROS), and its role is significant in the study of pulmonary arterial hypertension (PAH), a disease with poor prognosis.
- * Researchers found that TIGAR-deficient mice showed increased development of pulmonary hypertension when exposed to hypoxia, with heightened smooth muscle cell proliferation and autophagy compared to normal mice.
- * In vitro studies indicated that knocking down TIGAR in human pulmonary artery smooth muscle cells led to increased cell growth and ROS production, suggesting that targeting TIGAR could be a potential strategy for treating PAH.
Article Synopsis
- Sodium glucose co-transporter 2 inhibitors (SGLT2i), particularly ipragliflozin, are effective in slowing down the progression of diabetic kidney disease, as seen in various studies.
- Administering ipragliflozin to both type 2 and type 1 diabetic mice showed that it lowered blood glucose and urinary albumin levels, while also inhibiting kidney enlargement and reducing oxidative stress.
- The study highlighted that both high- and low doses of ipragliflozin protect kidney function by improving podocyte integrity and reducing renal tissue hypoxia, with dose-dependent effects particularly noted in the early stages of diabetic nephropathy.
Background: Energy starvation and the shift of energy substrate from fatty acids to glucose is the hallmark of metabolic remodeling during heart failure progression. However, ketone body metabolism in the failing heart has not been fully investigated.
Methods And Results: Microarray data analysis and mitochondrial isobaric tags for relative and absolute quantification proteomics revealed that the expression of D-β-hydroxybutyrate dehydrogenase I (Bdh1), an enzyme that catalyzes the NAD/NADH coupled interconversion of acetoacetate and β-hydroxybutyrate, was increased 2.
-Amino acids are enantiomers of L-amino acids and have recently been recognized as biomarkers and bioactive substances in mammals, including humans. In the present study, we investigated functions of the novel mammalian mitochondrial protein 9030617O03Rik and showed decreased expression under conditions of heart failure. Genomic sequence analyses showed partial homology with a bacterial aspartate/glutamate/hydantoin racemase.
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