NAMPT Is A Novel Inhibitor of Vascular Calcification in Chronic Kidney Disease.

Background: Vascular calcification is very common in patients with chronic kidney disease and contributes to the increased risk of cardiovascular events. NAMPT (nicotinamide phosphoribosyltransferase), the rate-limiting enzyme in the salvage pathway of nicotinamide adenine dinucleotide, has been shown to exert an antiaging effect on vascular smooth muscle cells. However, whether NAMPT is involved in the regulation of vascular calcification remains unclear.

NEXN protects against vascular calcification by promoting SERCA2 SUMOylation and stabilization.

Vascular calcification, a key risk factor for cardiovascular diseases, is driven by the phenotypic transition of vascular smooth muscle cells from a contractile to an osteogenic phenotype. NEXN, a protein highly associated with heart function, has also been implicated as a potential susceptibility factor in the development of coronary artery disease, but its role in the progression of vascular calcification remains unclear. In this study, multi-transcriptomics analysis and various animal models of male mice were used to explore the cell-specific roles and molecular mechanisms of NEXN in vascular calcification.

Genetic association between inflammatory factors and abdominal aortic calcification: Insights from a genome-wide association study.

Background: Current studies have indicated an association between inflammatory factor and vascular calcification. This study aimed to investigate the potential causal association between circulating inflammatory factor and abdominal aortic calcification (AAC) risk, and to identify potential drug targets for AAC.

Methods: We utilized genetic summary data for analysis, which included 91 circulating inflammatory factors from a genome-wide association study (GWAS) of 14,824 individuals of European descent, and AAC from a GWAS of 38,264 individuals of European descent from UK Biobank database.

TRIM16 Mediates K63-Linked Ubiquitination of DAB2 to Facilitate Vascular Calcification.

Background: Vascular calcification is highly prevalent in patients with chronic kidney disease (CKD), and the underlying mechanisms remain elusive. Several studies have indicated an important role of protein ubiquitination in vascular calcification. However, the role of E3 ubiquitin ligases in vascular calcification remains poorly understood.

GDF11 Alleviates Vascular Calcification in VitD-Overloaded Mice Through Inhibition of Inflammatory NF-κB Signal.

Vascular calcification, an age-associated disorder, is a highly regulated biological process similar to bone formation. Growth differentiation factor 11 (GDF11), a secreted member of the transforming growth factor beta (TGF-β) superfamily, has been shown to act as an anti-aging factor in the brain, heart, skin, and skeletal muscle. Nevertheless, whether GDF11 affects vascular calcification and the underlying mechanisms remain unclear.

The metabolite alpha-ketoglutarate inhibits vascular calcification partially through modulation of the TET2/NLRP3 inflammasome signaling pathway.

Introduction: Vascular calcification is prevalent in chronic kidney disease (CKD), but existing medical treatments fail to achieve satisfactory therapeutic effects. Vascular calcification is now recognized as an active multifactorial process involving diverse mechanisms. Alpha-ketoglutarate (AKG), an intermediate in tricarboxylic acid cycle, has been demonstrated to extend lifespan and ameliorate age-related osteoporosis.

Loss of ADAMTS5 promotes vascular calcification via versican/integrin β1/FAK signal.

Introduction: Extracellular matrix (ECM) proteases have been closely linked to the pathogenesis of vascular calcification. A disintegrin and metalloprotease with thrombospondin motifs-5 (ADAMTS5) is an ECM-degrading enzyme involved in ECM remodeling. Versican, a critical ECM component in the arteries, can be proteolytically cleaved by ADAMTS5 and activates integrin β1.

Honokiol attenuates oxidative stress and vascular calcification via the upregulation of heme oxygenase-1 in chronic kidney disease.

Vascular calcification (VC) is a common complication of chronic kidney disease (CKD), with oxidative stress identified as a key contributor to VC progression. Honokiol (HKL), a biphenolic compound derived from plants, has been found to be effective in treating various models of cardiovascular disease through the mitigation of oxidative stress. However, its effects on VC remain unexplored.

STING Facilitates Vascular Calcification via p-STAT1/NLRP3 Signal.

Vascular calcification is an independent predictor of cardiovascular mortality in patients with chronic kidney disease (CKD), yet no approved treatment exists. The cGAS-STING signaling participates in various cardiovascular diseases. Notably, DNA damage, an important regulator of vascular calcification, activates the cGAS-STING signaling.

Thrombospondin-1 binds to integrin β3 to inhibit vascular calcification through suppression of NF-κB pathway.

Vascular calcification is an important risk factor related to all-cause mortality of cardiovascular events in patients with chronic kidney disease (CKD). Vascular extracellular matrix (ECM) proteins have been demonstrated to regulate vascular calcification. ECM protein thrombospondin 1 (THBS1/TSP-1) plays a critical role in the regulation of vascular diseases.

4-Octyl itaconate inhibits vascular calcification partially via modulation of HMOX-1 signaling.

Vascular calcification frequently occurs in patients with chronic conditions such as chronic kidney disease (CKD), diabetes, and hypertension and represents a significant cause of cardiovascular events. Thus, identifying effective therapeutic targets to inhibit the progression of vascular calcification is essential. 4-Octyl itaconate (4-OI), a derivative of itaconate, exhibits anti-inflammatory and antioxidant activity, both of which play an essential role in the progression of vascular calcification.

Oxidized phospholipid POVPC contributes to vascular calcification by triggering ferroptosis of vascular smooth muscle cells.

Vascular calcification is an actively regulated biological process resembling bone formation, and osteogenic differentiation of vascular smooth muscle cells (VSMCs) plays a crucial role in this process. 1-Palmitoyl-2-(5'-oxo-valeroyl)-sn-glycero-3-phosphocholine (POVPC), an oxidized phospholipid, is found in atherosclerotic plaques and has been shown to induce oxidative stress. However, the effects of POVPC on osteogenic differentiation and calcification of VSMCs have yet to be studied.

The oxidized phospholipid PGPC impairs endothelial function by promoting endothelial cell ferroptosis via FABP3.

Ferroptosis is a novel cell death mechanism that is mediated by iron-dependent lipid peroxidation. It may be involved in atherosclerosis development. Products of phospholipid oxidation play a key role in atherosclerosis.

Wogonin inhibits oxidative stress and vascular calcification via modulation of heme oxygenase-1.

Vascular calcification (VC) is highly prevalent and increases the morbidity and mortality of cardiovascular diseases. However, the underlying mechanism remains unclear and there is no effective treatment so far. Interestingly, using systems pharmacology approach, we have predicted that Wogonin (Wog) exhibited potential activity against VC.

Sodium-glucose cotransporter 2 inhibitor canagliflozin alleviates vascular calcification through suppression of nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 inflammasome.

Aims: Vascular calcification (VC) is prevalent in pathological processes such as diabetes, chronic kidney disease (CKD), and atherosclerosis, but effective therapies are still lacking by far. Canagliflozin (CANA), a sodium-glucose cotransporter 2 inhibitor, has been approved for the treatment of type 2 diabetes mellitus and exhibits beneficial effects against cardiovascular disease. However, the effect of CANA on VC remains unknown.

Deletion of SIRT6 in vascular smooth muscle cells facilitates vascular calcification via suppression of DNA damage repair.

Vascular calcification is an important risk factor for cardiovascular events, accompanied by DNA damage during the process. The sirtuin 6 (SIRT6) has been reported to alleviate atherosclerosis, which is related to the reduction of DNA damage. However, whether smooth muscle cell SIRT6 mediates vascular calcification involving DNA damage remains unclear.

Repression of the antiporter SLC7A11/glutathione/glutathione peroxidase 4 axis drives ferroptosis of vascular smooth muscle cells to facilitate vascular calcification.

Vascular calcification is a common pathologic condition in patients with chronic kidney disease (CKD). Cell death such as apoptosis plays a critical role in vascular calcification. Ferroptosis is a type of iron-catalyzed and regulated cell death resulting from excessive iron-dependent reactive oxygen species and lipid peroxidation.

Downregulation of HDAC9 by the ketone metabolite β-hydroxybutyrate suppresses vascular calcification.

Vascular calcification is an actively regulated process resembling bone formation and contributes to the cardiovascular morbidity and mortality of chronic kidney disease (CKD). However, an effective therapy for vascular calcification is still lacking. The ketone body β-hydroxybutyrate (BHB) has been demonstrated to have health-promoting effects including anti-inflammation and cardiovascular protective effects.

Up-regulation of heme oxygenase-1 by celastrol alleviates oxidative stress and vascular calcification in chronic kidney disease.

Vascular calcification is very commonly observed in patients with chronic kidney disease (CKD), but there is no efficient therapy available. Oxidative stress plays critical roles in the progression of vascular calcification. Celastrol (Cel), a natural constituent derived from Chinese herbals, exhibits anti-oxidative stress activity.

Spermidine inhibits vascular calcification in chronic kidney disease through modulation of SIRT1 signaling pathway.

Vascular calcification is a common pathologic condition in patients with chronic kidney disease (CKD) and aging individuals. It has been established that vascular calcification is a gene-regulated biological process resembling osteogenesis involving osteogenic differentiation. However, there is no efficient treatment available for vascular calcification so far.

Erratum: Ion Therapy: A Novel Strategy for Acute Myocardial Infarction.

[This corrects the article DOI: 10.1002/advs.201801260.

25-Hydroxycholesterol promotes vascular calcification via activation of endoplasmic reticulum stress.

Vascular calcification is a highly regulated process similar to osteogenesis involving phenotypic change of vascular smooth muscle cells (VSMCs). 25-Hydroxycholesterol (25-HC), one of oxysterols synthesized by the enzyme cholesterol 25-hydroxylase, has been shown to promote bovine calcifying vascular cells (CVC) calcification. However, whether and how 25-HC regulates vascular calcification are not completely understood.