Elevated expression of periostin in diabetic cardiomyopathy and the effect of valsartan

Guan, Jun; Liu, Wenqi; Xing, Mingqing; Shi, Yue; Tan, Xueying; Jiang, Changqing; Dai, Hongji

doi:10.1186/s12872-015-0084-3

Cited by 36 publications

(35 citation statements)

References 30 publications

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“…Several previous studies have indicated a link between high glucose exposure and periostin expression [23,24]. In this study, we showed that ectopic expression of periostin prevented high glucose-induced apoptotic response in HUVECs, as determined by TUNEL staining and caspase-3 activity assay.…”

Section: Discussionsupporting

confidence: 54%

Upregulation of Periostin Prevents High Glucose-Induced Mitochondrial Apoptosis in Human Umbilical Vein Endothelial Cells via Activation of Nrf2/HO-1 Signaling

Zhong

Tang

2016

Cell Physiol Biochem

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Background/Aims: High glucose-induced oxidative damage to endothelial cells plays a central role in the pathogenesis of diabetic vascular complications. This study was undertaken to explore the role of periostin in high glucose-induced endothelial cell apoptosis and associated molecular mechanisms. Methods: Human umbilical vein endothelial cells (HUVECs) were exposed to high glucose (33.3 mmol/L) and examined for the expression of periostin. The effects of periostin upregulation on high glucose-induced apoptosis, mitochondrial dysfunction, and reactive oxygen species (ROS) production were determined. The activation of nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) by periostin was checked. HO-1 knockdown experiments were done to confirm its role in the action of periostin in high glucose-exposed HUVECs. Results: High glucose significantly upregulated the expression of periostin in HUVECs. Enforced expression of periostin attenuated high glucose-induced apoptosis in HUVECs, as determined by TUNEL staining and caspase-3 activity assay. Periostin overexpression prevented loss of Δψm, release of mitochondrial cytochrome c, and dysregulation of Bcl-2 and Bax in high glucose-exposed HUVECs. Periostin upregulation suppressed high glucose-induced ROS generation and activated the Nrf2/HO-1 signaling. HO-1 silencing restored high glucose-induced ROS generation and apoptotic response in periostin-overexpressing HUVECs. Conclusion: Periostin mitigates high glucose-induced mitochondrial apoptosis in endothelial cells, via activation of Nrf2/HO-1 signaling and reduction of ROS formation. Further studies are warranted to explore the therapeutic potential of periostin in diabetic vascular complications.

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Section: Discussionsupporting

confidence: 54%

Upregulation of Periostin Prevents High Glucose-Induced Mitochondrial Apoptosis in Human Umbilical Vein Endothelial Cells via Activation of Nrf2/HO-1 Signaling

Zhong

Tang

2016

Cell Physiol Biochem

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“…Lower periostin levels may suggest a reduced ability to undergo adaptive ventricular remodelling among patients with diabetes compared with patients without diabetes. In previous rat studies of diabetic cardiomyopathy, myocardial expression of periostin was higher . The finding of lower periostin in our study may reflect differences in location of periostin measurement (serum vs. myocardium) or clinical state (acute vs. chronic HF).…”

Section: Discussionsupporting

confidence: 41%

“…Our results extend upon work from existing experimental models. In diabetic rats, compared with controls, periostin is closely associated with ventricular fibrosis and adverse cardiac remodelling . The use of valsartan in diabetic rats significantly improved ventricular remodelling and markers of fibrosis by possibly targeting the periostin pathway .…”

Section: Discussionmentioning

confidence: 97%

A network analysis to compare biomarker profiles in patients with and without diabetes mellitus in acute heart failure

Sharma

Demissei

Tromp

et al. 2017

European J of Heart Fail

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AimsIt is unclear whether distinct pathophysiologic processes are present among patients with acute heart failure (AHF), with and without diabetes. Network analysis of biomarkers may identify correlative associations which reflect different pathophysiologic pathways. Methods and resultsWe analyzed a panel of 48 circulating biomarkers measured within 24 hours of admission for AHF in a subset of patients enrolled in the PROTECT trial. In patients with and without diabetes, we performed a network analysis to identify correlations between measured biomarkers. Compared to patients without diabetes (n=1111), those with diabetes (n=922) had higher prevalence of ischemic heart disease and traditional coronary risk factors. Patients with and without diabetes, after multivariable adjustment, had significantly different levels of biomarkers across a spectrum of pathophysiologic domains including inflammation (TNF-1a, periostin), cardiomyocytes stretch (BNP), angiogenesis (VEGFR, angiogenin), and renal function (NGAL, KIM-1) (adjusted p-value <0.05). Among patients with diabetes, network analysis revealed that periostin strongly clustered with C-reactive protein and interleukin-6. Furthermore, renal markers (creatinine and NGAL) closely associated with potassium and glucose. These findings were not seen among patients without diabetes ConclusionPatients with AHF and diabetes, compared to those without diabetes, have distinct biomarker profiles. Network analysis suggests that cardiac remodeling, inflammation, and fibrosis are closely associated with each other in patients with diabetes; Furthermore, potassium levels may be sensitive to changes in renal function as reflected by the strong renal-potassiumglucose correlation. These findings were not seen among patients without diabetes and may suggest distinct pathophysiologic processes among patients with diabetes.

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“…Periostin was significantly elevated along with other TGF markers, such as TGF‐β1, TGF‐β1 R II, and Type I and III collagens in the myocardium of diabetic rats compared with control group . In streptozotocin (STZ)‐induced type 1 diabetic mice model, enhanced reactive oxygen species (ROS) production, activation of extracellular regulated kinase (ERK), TGF‐β, periostin pathway, and myocardial fibrosis resulted in important consequences in mice with DCM.…”

Section: Resultsmentioning

confidence: 99%

Periostin as a novel biomarker of cardiovascular disease: A systematic evidence landscape of preclinical and clinical studies

Azharuddin

Adil

Ghosh

et al. 2019

J Evidence Based Medicine

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Background Periostin is a matricellular protein, expressed in various normal adult and fetal tissues. Recently, elevated periostin levels have been reported in heart failure, coronary artery disease, and stroke. However, there is lack of clinical studies to clarify the prognostic significance of systemic periostin levels in cardiovascular diseases (CVDs). The aim of the study was to perform a systematic review of published evidence on periostin and CVDs, and to clarify the diagnostic and prognostic significance of systemic periostin levels in CVDs. Methods A systematic search on PubMed was performed to identify relevant articles from inception to December 2018. The eligible studies evaluating the periostin expression and periostin levels in animal and human studies. Results A total of 24 relevant studies, including both animal and human data, were included. Periostin is significantly observed in myocardium tissue of failing hearts compared with control, and is also expressed in atherosclerotic plaques. Systemic periostin levels were significantly correlated with cardiac function and severity of CVD in several studies. A clinical study also observed positive correlation between periostin and N‐terminal pro b‐type natriuretic peptide (NT‐proBNP), highly sensitive troponin (hsTnT), and ST2 cardiac biomarker. Studies reported limited adjustment for potential confounders. Conclusions The evidence of current review support potential role of periostin in the pathophysiology of CVD. However, scarcity of data regarding the clinical use of periostin levels in the current management of CVDs further creates room for the future investigation. Therefore, further studies warrant to clarify its potential role, if any, as a novel cardiac biomarker.

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Elevated expression of periostin in diabetic cardiomyopathy and the effect of valsartan

Cited by 36 publications

References 30 publications

Upregulation of Periostin Prevents High Glucose-Induced Mitochondrial Apoptosis in Human Umbilical Vein Endothelial Cells via Activation of Nrf2/HO-1 Signaling

Upregulation of Periostin Prevents High Glucose-Induced Mitochondrial Apoptosis in Human Umbilical Vein Endothelial Cells via Activation of Nrf2/HO-1 Signaling

A network analysis to compare biomarker profiles in patients with and without diabetes mellitus in acute heart failure

Periostin as a novel biomarker of cardiovascular disease: A systematic evidence landscape of preclinical and clinical studies

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