Publications by authors named "Fangyan Tan"

Renal ischemia-reperfusion injury (IRI) is a common clinical condition that currently lacks effective treatment options. Inhibitors targeting the sodium-glucose co-transporter-2 (SGLT-2), recognized for their role in managing hyperglycemia, have demonstrated efficacy in enhancing the health outcomes for diabetic patients grappling with chronic kidney disease. Nevertheless, the precise impact of SGLT-2 inhibitors on renal ischemia-reperfusion injury (IRI) and the corresponding transcriptomic alterations remain to be elucidated.

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Background: Ulcerative colitis (UC) is a chronic, recurrent, non-specific inflammatory disease, and the pathogenesis of the disease remains unclear. Ferroptosis is a form of programmed cell death characterized by the accumulation of iron-dependent lipid peroxides, which are simultaneously closely related to reactive oxygen species (ROS). Although seliciclib is highly effective against immune inflammation, its mechanism on colitis is unclear.

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Damage to the heart can start the repair process and cause cardiac remodeling. B cells play an important role in this process. B cells are recruited to the injured place and activate cardiac remodeling through secreting antibodies and cytokines.

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An early and accurate diagnosis of septic cardiomyopathy is vital for improving the overall prognosis of sepsis. In our research, we aimed to identify signature genes and their immune connections in septic cardiomyopathy. By analyzing the mouse myocardial transcriptome from sepsis induced by cecum ligation and puncture (CLP), we identified four distinct k-means clusters.

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Sodium-glucose cotransporter 2 inhibitors (SGLT2i) represent an innovative class of antidiabetic agents that have demonstrated promise in mitigating cardiac remodeling. However, the transcriptional regulatory mechanisms underpinning their impact on blood pressure and the reversal of hypertension-induced cardiac remodeling remain largely unexplored. Given this context, our study concentrated on comparing the cardiac expression profiles of lncRNAs and mRNAs between Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).

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Article Synopsis
  • - Ferroptosis, linked to lipid buildup in cells, worsens acute kidney injury (AKI), but how this happens is not well understood.
  • - In a study using mouse models and AKI patients, researchers found that reducing a protein called augmenter of liver regeneration (ALR) increased ferroptosis and damage to mitochondria while overexpressing ALR reduced these effects.
  • - The study revealed that ALR interacts with another protein, ACSL4, to lower levels of harmful fatty acids and protect against ferroptosis, suggesting that enhancing ALR could be an effective approach for treating AKI.
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Reactive oxidative species (ROS) production-driven ferroptosis plays a role in acute kidney injury (AKI). However, its exact molecular mechanism is poorly understood. Scavenger receptor CD36 has important roles in oxidizing lipids, lipid accumulation, metabolic syndrome, and insulin resistance in chronic kidney disease, but its roles remain unexplored in AKI.

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Article Synopsis
  • Sodium-glucose co-transporter-2 inhibitors (SGLT2i) like empagliflozin are effective in reducing cardiovascular disease and improving kidney health in diabetic patients, but their specific effects on hypertensive individuals need more research.
  • This study used RNA sequencing to explore how empagliflozin affects gene expression in various tissues (like the kidney and lungs) in hypertensive rats, alongside blood pressure measurements to validate the findings.
  • Results showed significant changes in gene expression linked to blood pressure and metabolism regulation, with evidence of reduced pro-inflammatory factors and increased anti-inflammatory markers after empagliflozin treatment.
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Article Synopsis
  • * SGLT2 inhibitors like dapagliflozin (DAPA) have been shown to improve outcomes in patients with chronic kidney disease and diabetes, but how DAPA works is not fully understood.
  • * In a study using spontaneously hypertensive rats, it was found that DAPA treatment for 8 weeks positively impacted kidney health by affecting gene expression related to metabolism and inflammation, highlighting Zbtb20 as a potential therapeutic target.
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Necroptosis plays an important role in the pathogenesis of acute kidney injury (AKI), and necroptosis-related interventions may therefore be an important measure for the treatment of AKI. Our previous study has shown that augmenter of liver regeneration (ALR) inhibits renal tubular epithelial cell apoptosis and regulates autophagy; however, the influence of ALR on necroptosis remains unclear. In this study, we investigated the effect of ALR on necroptosis caused by ischemia-reperfusion and the underlying mechanism.

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