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lu, w.

Publications and source records attributed to lu, w..

2 recordsLinked to original sources

Non-planar perylene diimides dual-targeting mitochondrial membrane potential and mitochondrial DNA transcription for an-titumor Therapy

Mitochondrial DNA (mtDNA) transcription is an emerging target in cancer therapy. While enzyme-targeted inhibitors such as IMT1B block POLRMT, their organelle specificity remains unclear. Here, we report a distinct strategy using non-planar perylene diimide derivatives (PDIs). The fluorescent lead compound PDIC-BL combines mitochondrial membrane potential ({Delta}{Psi}m) dependent accumulation (validated in cells and isolated mitochondria), and with direct intercalation into mtDNA (Kd = 32 M), as demonstrated by single-molecule stretching assays. This dual-targeting mechanism leads to selective inhibition of mitochondrial transcription, ROS generation and triggers apoptosis. PDIC-BL exhibits superior antitumor efficacy in breast cancer cell lines (MCF-7, MDA-MB-231) and significantly supresses tumor growth in vivo, with good tolerability in cancer xenograft model in nude mice. This work not only elucidates the structure-activity relationship of non-planar PDIs, but also offers a generalizable strategy for developing organelle-selective DNA binding therapeutics.

cancer biology↗

Nephrectomy and high-salt diet inducing pulmonary hypertension and kidney damage by increasing Ang II concentration in rats

BackgroundPulmonary hypertension (PH) is a common complication in patients with chronic kidney disease (CKD), affecting prognosis. However, the pathogenesis is not clear, and the lack of a stable animal model is a significant factor. MethodsIn this study, a rat model of chronic kidney disease with pulmonary hypertension (CKD-PH) was developed through 5/6 nephrectomy combined with a high-salt diet. The models hemodynamics and pathological changes in multiple organs were dynamically assessed. Lung tissues and serum were collected from the model rats to measure the expression of ACE2, the expression levels of vascular active components related to the renin-angiotensin-aldosterone system (RAAS), and changes in the serum metabolic profile of the model. ResultsAfter 14 weeks post-surgery, the CKD-PH rat model exhibited significant changes in hemodynamic parameters indicative of pulmonary arterial hypertension, along with alterations such as right ventricular hypertrophy. However, no evidence of pulmonary vascular remodeling was observed. An imbalance in the renin-angiotensin-aldosterone system was identified in the CKD-PH rat models. Downregulation of ACE2 expression was observed in pulmonary tissues. The serum metabolic profile of the CKD-PH rat models showed distinct differences compared to the sham surgery group. ConclusionsThe development of pulmonary arterial hypertension in CKD-PH rats may be primarily attributed to the disruption of the renin-angiotensin-aldosterone system (RAAS), coupled with a decrease in ACE2 expression in pulmonary vascular endothelial tissues and metabolic disturbances.

pathology↗