Although macrophage infiltration has been proven to increase calcified artery media in chronic kidney disease (CKD) patients, the mechanism by which macrophages are involved in vascular calcification (VC) progression remains unclear. Taking advantage of miRNA-seq, RNA-seq, dual-luciferase reporter assay, qRT-PCR, and arteries from CKD patients as well as CKD mouse models, we identified that high-phosphate-stimulated macrophage-derived exosomes (Mexo-P) suppressed let-7b-5p expression in VSMCs, which further upregulated TGFBR1. Moreover, gain-and-loss-of-function assays were used to determine the regulatory effects and downstream mechanism of let-7b-5p and TGFBR1 on VC. Mechanically, Mexo-P induced VSMC TGFBR1 upregulation by suppressing let-7b-5p, which further amplifies SMAD3/RUNX2 signaling and thereby contributes to VC. Our findings indicate that macrophage-derived exosomes promote CKD-associated VC through the let-7b-5p/TGFBR1 axis in high-phosphate conditions. Our study provides insight into macrophages associated with VC, which might be potential therapeutical targets for VC.

Immune cells play a key role in maintaining renal dynamic balance and dealing with renal injury. The physiological and pathological functions of immune cells are intricately connected to their metabolic characteristics. However, immunometabolism in chronic kidney disease (CKD) is not fully understood. Pathophysiologically, disruption of kidney immune cells homeostasis causes inflammation and tissue damage via triggering metabolic reprogramming. The diverse metabolic characteristics of immune cells at different stages of CKD are strongly associated with their different pathological effect. In this work, we reviewed the metabolic characteristics of immune cells (macrophages, natural killer cells, T cells, natural killer T cells and B cells) and several non-immune cells, as well as potential treatments targeting immunometabolism in CKD. We attempt to elaborate on the metabolic signatures of immune cells and their intimate correlation with non-immune cells in CKD.

Deubiquitinases are a group of proteins that identify and digest monoubiquitin chains or polyubiquitin chains attached to substrate proteins, preventing the substrate protein from being degraded by the ubiquitin-proteasome system. Deubiquitinases regulate cellular autophagy, metabolism and oxidative stress by acting on different substrate proteins. Recent studies have revealed that deubiquitinases act as a critical regulator in various cardiac diseases, and control the onset and progression of cardiac disease through a board range of mechanism. This review summarizes the function of different deubiquitinases in cardiac disease, including cardiac hypertrophy, myocardial infarction and diabetes mellitus-related cardiac disease. Besides, this review briefly recapitulates the role of deubiquitinases modulators in cardiac disease, providing the potential therapeutic targets in the future.

High-flow vascular access is one of the serious complications in the maturation and subsequent use of arteriovenous fistula (AVF). We adopted a novel surgical approach named no incision limited ligation indwelling needle assisted- revision (NILLINR) to treat high-flow of the hemodialysis vascular access and ascertained the outcomes by regular follow-up visits. This is a retrospective study. 26 hemodialysis patients with symptomatic high-flow access (access flow > 1500 mL/min) were treated with the novel banding method without incision between June 2018 and October 2020. The flow of the brachial artery before and after the restriction was measured by experienced clinicians by using the duplex Doppler ultrasound (DUS). All 26 patients were followed up for up to 1 year. Meanwhile, the brachial artery flow was recorded at 6 months and 1 year after restriction. Of all 26 patients included in this study, the mean access flow volume decreased from 2196.2 ± 416.9 mL/min (mean ± SD) to 679.2 ± 67.1 mL/min immediately after the operation. During the follow-up, the volume flow of the brachial artery was still within the restricted range at 6 months (mean ± SD, 720.2 ± 164.7 mL/min) and 1 year (mean ± SD, 713.9 ± 173.8 mL/min) after the operation. Meanwhile, the mean duration of the operation is 8.5 ± 3.3 min, and there is no bleeding or rupture. This novel no-incision limited ligation indwelling needle-assisted revision is a safe, effective, and time-saving option to treat high-flow access.