Exploring the Communal Pathogenesis, Ferroptosis Mechanism, and Potential Therapeutic Targets of Dilated Cardiomyopathy and Hypertrophic Cardiomyopathy via a Microarray Data Analysis

Wang, Zuoxiang; Xia, Qingyue; Su, Wenxing; Cao, Mingqiang; Sun, Yunjuan; Zhang, Mingyang; Chen, Weixiang; Jiang, Tingbo

doi:10.3389/fcvm.2022.824756

Cited by 19 publications

(15 citation statements)

References 72 publications

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“…Another annotation term that was up-regulated in LVRR- vs LVRR+ patients was the cell adhesion. Cell adhesion pathways have been found to be dysregulated on the transcriptome level in the DCM heart tissue. , …”

Section: Discussionmentioning

confidence: 99%

“…Cell adhesion pathways have been found to be dysregulated on the transcriptome level in the DCM heart tissue. 51,52 The most prominent among the proteins up-regulated in the nonresponding LVRR− patients was fructose-bisphosphate aldolase B (ALDOB). In a study by Rueda et al 53 ALDOB was used as one of four proteins to predict the low-term risk of mortality in patients with cardiogenic shock.…”

Section: ■ Discussionmentioning

confidence: 99%

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Proteomic Profiling of Dilated Cardiomyopathy Plasma Samples ─ Searching for Biomarkers with Potential to Predict the Outcome of Therapy

Klimentova,

Rehulka,

Stulik

et al. 2024

J. Proteome Res.

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Determination of the prognosis and treatment outcomes of dilated cardiomyopathy is a serious problem due to the lack of valid specific protein markers. Using in-depth proteome discovery analysis, we compared 49 plasma samples from patients suffering from dilated cardiomyopathy with plasma samples from their healthy counterparts. In total, we identified 97 proteins exhibiting statistically significant dysregulation in diseased plasma samples. The functional enrichment analysis of differentially expressed proteins uncovered dysregulation in biological processes like inflammatory response, wound healing, complement cascade, blood coagulation, and lipid metabolism in dilated cardiomyopathy patients. The same proteome approach was employed in order to find protein markers whose expression differs between the patients well-responding to therapy and nonresponders. In this case, 45 plasma proteins revealed statistically significant different expression between these two groups. Of them, fructose-1,6-bisphosphate aldolase seems to be a promising biomarker candidate because it accumulates in plasma samples obtained from patients with insufficient treatment response and with worse or fatal outcome. Data are available via ProteomeXchange with the identifier PXD046288.

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Section: Discussionmentioning

confidence: 99%

Section: ■ Discussionmentioning

confidence: 99%

Proteomic Profiling of Dilated Cardiomyopathy Plasma Samples ─ Searching for Biomarkers with Potential to Predict the Outcome of Therapy

Klimentova,

Rehulka,

Stulik

et al. 2024

J. Proteome Res.

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“…The leading cause of Friedreich's ataxia-related death is HCM, which is attenuated by the combined therapy of idebenone and oral low-dose deferiprone [64,65]. Microarray data analysis showed that some ferroptosis genes are associated with HCM, such as ATF3, LPCAT3, and solute carrier family 1 member 5 (SLC1A5) [66]. Diabetic Cardiomyopathy DCM is a pathophysiological condition caused by diabetes that contributes to HF where the decline of myocardial cell function is an important mediating mechanism [67].…”

Section: Iron Overload Cardiomyopathymentioning

confidence: 99%

“…The leading cause of Friedreich’s ataxia-related death is HCM, which is attenuated by the combined therapy of idebenone and oral low-dose deferiprone [64, 65]. Microarray data analysis showed that some ferroptosis genes are associated with HCM, such as ATF3, LPCAT3, and solute carrier family 1 member 5 (SLC1A5) [66].…”

Section: Ferroptosis and Cvdmentioning

confidence: 99%

A Panoramic View of Ferroptosis in Cardiovascular Disease

Cheng¹,

Yu²,

Yang³

et al. 2023

Kidney Dis

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Background: Cardiovascular disease (CVD) remains the leading cause of disease burden worldwide. Ferroptosis, an iron-dependent form of programmed cell death, is characterized by the lethal accumulation of lipid peroxidation, which is morphologically, biochemically and genetically distinct from apoptosis, necrosis and pyroptosis. Emerging evidence provides exciting novel insights to allow for a deeper understanding of the physiology and pathology of ferroptosis in CVD. Summary: The rapidly evolving insights into ferroptosis have revealed its role in the pathogenesis of diverse forms of CVD, including cardiomyopathy, heart failure, atherosclerosis, pulmonary arterial hypertension and cerebrovascular disease. Various types of metabolic pathways are involved in the regulation of ferroptosis, including iron metabolism, lipid metabolism and oxidative metabolism. Modulators of ferroptosis, such as several clinical drugs, preclinical compounds and other emerging materials, have been applied as promising approaches in the prevention and treatment of CVD. Key message: In this review, we provide a 360-degree view of the latest progress in the field of ferroptosis in CVD, highlight the pathogenic role of ferroptosis in CVD and also discuss the importance and future directions of targeting ferroptosis in CVD.

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“…Second, STAT3 is the direct target of miRNA. Some miRNA predicted to target STAT3, which is an inhibitor of ferroptosis in DCM ( 37 ). In summary, STAT3-miRNA protects the heart against DCM.…”

Section: Stat3-mirna Crosstalk In Dilated Cardiomyopathymentioning

confidence: 99%

The crosstalk between STAT3 and microRNA in cardiac diseases and protection

Li²,

Li³

2022

Front. Cardiovasc. Med.

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Signal transducer and activator of transcription 3 (STAT3), an important transcription factor and signaling molecule, play an important role in cardiac disease and protection. As a transcription factor, STAT3 upregulates anti-oxidative and anti-apoptotic genes but suppresses anti-inflammatory and anti-fibrotic genes in cardiac disease and protection. As a signaling molecule, STAT3 is the downstream or upstream of other molecules for signaling transduction, also activated in cardiac disease and protection. MicroRNAs (miRNAs) are endogenous short non-coding RNAs that regulate mRNA expression at the transcriptional level and prevent protein translation. Recently, STAT3 is reported to be not only the target of miRNA but also the inhibitor or inducer of miRNA to modify the mRNA expression profiles in cardiomyocytes resulting in different effects on cardiac disease and protection. We summarize the current knowledge on STAT3 regulation of individual miRNAs and the modulation of STAT3 by miRNAs in cardiac diseases and protection.

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Exploring the Communal Pathogenesis, Ferroptosis Mechanism, and Potential Therapeutic Targets of Dilated Cardiomyopathy and Hypertrophic Cardiomyopathy via a Microarray Data Analysis

Cited by 19 publications

References 72 publications

Proteomic Profiling of Dilated Cardiomyopathy Plasma Samples ─ Searching for Biomarkers with Potential to Predict the Outcome of Therapy

Proteomic Profiling of Dilated Cardiomyopathy Plasma Samples ─ Searching for Biomarkers with Potential to Predict the Outcome of Therapy

A Panoramic View of Ferroptosis in Cardiovascular Disease

The crosstalk between STAT3 and microRNA in cardiac diseases and protection

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