Induction of intracellular heat-shock protein 72 prevents the development of vascular smooth muscle cell calcification

Lu, Tzongshi; Lim, Kenneth; Molostvov, Guerman; Yang, Yi; Yiao, Szu-Yu; Zehnder, Daniel; Hsiao, Li‐Li

doi:10.1093/cvr/cvs278

Cited by 9 publications

(12 citation statements)

References 36 publications

(31 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, the low expression of HSP70 in the arterial wall is associated with an increased risk of vascular calcification (Lu et al. 2012 ). However, it was also reported that extracellular HSP70 could promote BMP2/4-induced cell condensation and osteogenic differentiation in calcifying vascular cells by binding with matrix GLA protein (Yao et al.…”

Section: Discussionmentioning

confidence: 99%

“…The expression of HSP70 is compromised in CKD patients with coronary artery disease (CAD), and induction of intracellular HSP70 could prevent the development of VSMC calcification (Lu et al. 2012 ). Downregulation of HSP90 was also found in calcified aortic valves, suggesting HSP90 as a central signalling molecule in aortic valvular calcification (Weisell et al.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Aspirin relieves the calcification of aortic smooth muscle cells by enhancing the heat shock response

Shen

Chen

Liu

et al. 2021

Pharmaceutical Biology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Aspirin relieves the calcification of aortic smooth muscle cells by enhancing the heat shock response

Shen

Chen

Liu

et al. 2021

Pharmaceutical Biology

View full text Add to dashboard Cite

“…Lu et al demonstrated that HSP72 induction can prevent the development of vascular calcification in human aortic smooth muscle cells [104]. Vascular calcification is correlated with cardiovascular mortality and is commonly observed in patients with coronary artery disease and CKD initiated by CRS type 4 [105,106].…”

Section: Role Of Hsps In Cardiorenal Syndromementioning

confidence: 99%

Heat Shock Proteins: Connectors between Heart and Kidney

Junho

Azevedo

Cunha

et al. 2021

Cells

View full text Add to dashboard Cite

Over the development of eukaryotic cells, intrinsic mechanisms have been developed in order to provide the ability to defend against aggressive agents. In this sense, a group of proteins plays a crucial role in controlling the production of several proteins, guaranteeing cell survival. The heat shock proteins (HSPs), are a family of proteins that have been linked to different cellular functions, being activated under conditions of cellular stress, not only imposed by thermal variation but also toxins, radiation, infectious agents, hypoxia, etc. Regarding pathological situations as seen in cardiorenal syndrome (CRS), HSPs have been shown to be important mediators involved in the control of gene transcription and intracellular signaling, in addition to be an important connector with the immune system. CRS is classified as acute or chronic and according to the first organ to suffer the injury, which can be the heart (CRS type 1 and type 2), kidneys (CRS type 3 and 4) or both (CRS type 5). In all types of CRS, the immune system, redox balance, mitochondrial dysfunction, and tissue remodeling have been the subject of numerous studies in the literature in order to elucidate mechanisms and propose new therapeutic strategies. In this sense, HSPs have been targeted by researchers as important connectors between kidney and heart. Thus, the present review has a focus to present the state of the art regarding the role of HSPs in the pathophysiology of cardiac and renal alterations, as well their role in the kidney–heart axis.

show abstract

“…To date, in vitro and in vivo experiments have tested 12 natural antioxidants that are also dietary ingredients, including 10-dehydrogingerdione (10-DHGD) 64 , apocynin 18,19 , curcumin 38 , diosgenin 20,21 , ellagic acid 56 , gallic acid 48 , gingko biloba extracts 50 , puerarin 62 , quercetin 25–31 , resveratrol 52 , silybin 38 , and vitamin E 34,35 . Among these compounds, apocynin, diosgenin, quercetin, and vitamin E have been shown by multiple studies to have anti-VC properties.…”

Section: Antioxidants From Natural and Dietary Sources For Treatment mentioning

confidence: 99%

“…It has been extensively investigated with respect to its effect against VC based on our literature search results. Lu et al disclosed that quercetin abolished heat shock protein 72 induced anti-calcification effect in vitro and ex vivo 25 ; however, another group later found that quercetin completely nullified warfarin-induced aortic calcification and aortic medial cartilaginous metaplasia by inhibiting transglutaminase 2 and β-catenin expression in vitro 26–28 . Alternatively, quercetin could reduce aortic calcification in CKD rats partially by increasing superoxide dismutase 2 (SOD2) levels and modulating the inducible NO synthase (iNOS)/MAPK pathway 29 .…”

Section: Antioxidants From Natural and Dietary Sources For Treatment mentioning

confidence: 99%

Natural and non-natural antioxidative compounds: potential candidates for treatment of vascular calcification

et al. 2019

View full text Add to dashboard Cite

Vascular calcification (VC) is highly prevalent in patients with advanced age, or those with chronic kidney disease and diabetes, accounting for substantial global cardiovascular burden. The pathophysiology of VC involves active mineral deposition by transdifferentiated vascular smooth muscle cells exhibiting osteoblast-like behavior, building upon cores with or without apoptotic bodies. Oxidative stress drives the progression of the cellular phenotypic switch and calcium deposition in the vascular wall. In this review, we discuss potential compounds that shield these cells from the detrimental influences of reactive oxygen species as promising treatment options for VC. A comprehensive summary of the current literature regarding antioxidants for VC is important, as no effective therapy is currently available for this disease. We systematically searched through the existing literature to identify original articles investigating traditional antioxidants and novel compounds with antioxidant properties with regard to their effectiveness against VC in experimental or clinical settings. We uncovered 36 compounds with antioxidant properties against VC pathology, involving mechanisms such as suppression of NADPH oxidase, BMP-2, and Wnt/β-catenin; anti-inflammation; and activation of Nrf2 pathways. Only two compounds have been tested clinically. These findings suggest that a considerable opportunity exists to harness these antioxidants for therapeutic use for VC. In order to achieve this goal, more translational studies are needed.

show abstract

Induction of intracellular heat-shock protein 72 prevents the development of vascular smooth muscle cell calcification

Abstract: Our study shows for the first time that intracellular HSP72 may function as a central regulator of molecular pathways involved in the development of VC. We suggest treatment strategies that up-regulate HSP72 as a new approach to inhibit VC.

Cited by 9 publications

References 36 publications

Aspirin relieves the calcification of aortic smooth muscle cells by enhancing the heat shock response

Aspirin relieves the calcification of aortic smooth muscle cells by enhancing the heat shock response

Heat Shock Proteins: Connectors between Heart and Kidney

Natural and non-natural antioxidative compounds: potential candidates for treatment of vascular calcification

Contact Info

Product

Resources

About