RETRACTED: Downregulation of microRNA‐23b protects against ischemia‐reperfusion injury via p53 signaling pathway by upregulating MDM4 in rats

Zhao, Zhi; Guan, Jianzhong; Wu, Min; Lai, Gui-Hua; Zhu, Zhonglian

doi:10.1002/jcb.27748

Cited by 11 publications

(10 citation statements)

References 26 publications

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“…Compared with health control, only MDM4 was signi cantly overexpressed (FC = 1.0495, p = 0.0037) in ischemic group, while the four signature genes did not signi cantly change in ischemic cardiomyopathy group. It matches the previously reports that the upregulated MDM4 plays cardio-protective effect in ischemia-refuse injury 50 . Overexpression of MDM4 re ects the self-correction of physiological system in abnormal physiological condition of ischemic.…”

Section: Discussionsupporting

confidence: 93%

Novel Signature Genes for Human Left Ventricle Cardiomyopathies Identified by Weighted Co-expression Network Analysis (WGCNA)

Tian¹,

Wu²,

Zhang³

et al. 2020

Preprint

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BackgroundCardiomyopathy, a heart disease that arises from different etiologies, brings a huge healthcare burden to the global society. Identification of biomarkers can be very useful for early diagnosis of cardiomyopathy, interruption of the disease procession to heart failure, and decrement of the mortality. MethodsClinical cases of cardiomyopathy were screened out of independently investigations from the genomic database. Exploration of its whole transcription disorder pattern by WGCNA (Weighted Gene Co-expression Network Analysis) to discover the signature genes for different subtypes of cardiomyopathy. The hub genes and key pathways, which are correlated to cardiomyopathy traits, were identified through co-expression and protein-protein interaction (PPI) networks enrichment analysis. Discovered hub genes were blast through the Cardiovascular Disease Portal to verify functions related to human cardiomyopathies.ResultsThree common axes of signature genes were discovered for five subtypes of cardiomyopathy: 1) Four genes (MDM4, CFLAR, RPS6KB1, PKD1L2) were common for ischemic and ischemic cardiomyopathy subgroups; 2) Subtypes of cardiomyopathy (ischemic, post. partum, familiar and idiopathic) shared eight genes (MAPK1, MAPK11, MAPK14, LMNA, RAC1, PECAM1, XIAP, CREB1); 3) TFAM and RHEB were the common signature genes for subtypes of cardiomyopathy (viral, post. partum, familiar, and idiopathic). Major pathways enriched were including MAPK signaling pathway, the pathway of protein processing in endoplasmic reticulum, and pathway of regulatory actin cytoskeleton. Aberrant in these pathways caused disorders metabolic process and cellular malfunctions that generally contributes to cardiac dysregulation and functional relapse into cardiomyopathies.ConclusionThis study identified the key signaling pathways, functions and biological process related to cardiomyopathies and will give a light to better understand the molecular mechanism of processes of cardiomyopathies and figure out the rational clinical interference way to cure the patients. Therein, these novel signature genes may work as potential promising biomarkers for cardiomyopathy diagnosis, and will benefit for the better clinical diagnostics and outcome for patients with cardiomyopathies.

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Section: Discussionsupporting

confidence: 93%

Novel Signature Genes for Human Left Ventricle Cardiomyopathies Identified by Weighted Co-expression Network Analysis (WGCNA)

Tian¹,

Wu²,

Zhang³

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…Compared between health and ischemic groups, only MDM4 was signi cantly overexpressed (FC = 1.0495, p = 0.0037) in ischemic group, while the four signature genes did not signi cantly change in ischemic cardiomyopathy group. It matches the previously reports that the upregulated MDM4 plays cardio-protective effect in ischemia -refuse injury [47]. Overexpression of MDM4 re ects the selfcorrection of physiological system in abnormal physiological condition of ischemic.…”

Section: Discussionsupporting

confidence: 91%

Co-expression network analysis identified novel potential Signature Genes Associated with human left ventricle cardiomyopathies arises from different etiologies

Tian¹,

Wu²,

He³

et al. 2020

Preprint

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Abstract Background: Heat disease is worldwide pandemic and brings huge healthcare burden to global society. However, it is still illusive that the whole transcription disorder pattern of cardiomyopathies arises from different etiologies. We applied Weighted Gene Co-Expression Network Analysis (WGCNA) to construct and screen functional gene significantly related to 8 subtypes of cardiomyopathies. Through co-expression and protein-protein interaction (PPI) networks enrichment analysis, the hub genes and key pathways were identified, which highly correlated with pathologic traits. Compared with expression profile of healthy group, potential disease signature genes were validated through another independently investigations of cardiomyopathies via cardiovascular disease bioportal. Results: The novel potential disease signature genes were identified and assembled into three axes that shared among five cardiomyopathies groups, including idiopathic cardiomyopathy, familial cardiomyopathy, post-partum cardiomyopathy, Ischemic cardiomyopathy and viral cardiomyopathy. Four disease signature genes (MDM4, CFLAR, RPS6KB1, PKD1L2) were shared by ischemic and ischemic cardiomyopathy group. Eight signature genes (MAPK1, MAPK11, MAPK14, LMNA, RAC1, PECAM1, XIAP, CREB1) were overlapped by Ischemic Cardiomyopathy with Post. Partum/Familiar/Idiopathic Cardiomyopathy groups. The signature genes (TFAM, RHEB) were common genes among Viral Cardiomyopathy and Post. Partum / Familiar /Idiopathic Cardiomyopathy groups. These some novel signature genes were highlighted as potential biomarkers for cardiomyopathies. The majority disorder functions and pathways enriched in metabolic processes and concentrated on MAPK signaling pathway, protein processing in endoplasmic reticulum, regulation of actin cytoskeleton pathway. Conclusion: It strongly suggests that expression disorder of these signature genes may contribute the cardiac dysregulation and relapse into cardiomyopathies. Taken together, these novel signature genes could be utilized as diagnostic biomarkers or therapy targets and benefit the precise clinical diagnostics with better outcome. In summary, this study will attract great interest of clinical research scientists as well as medical scientists that work on heart diseases.

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“…Moreover, knockdown of miR-23b also contributed to attenuated IBI in mouse tissues in vivo. Consistent with our study, the inhibition of miR-23b resulted in the upregulation of murine double minute 4 in rats through p53 signaling pathway, thereby protecting against ischemia-reperfusion (IR) injury [39]. The myocardial function disrupted by IR injury could be reversed following the suppression of miR-23b expression [40].…”

Section: Discussionsupporting

confidence: 79%

Downregulation of miR-23b by transcription factor c-Myc alleviates ischemic brain injury by upregulating Nrf2

Xin

et al. 2021

Int. J. Biol. Sci.

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Ischemic brain injury (IBI) is a common acute cerebral vessel disease that occurs secondary to blockage in arteries, mainly characterized by insufficient blood supply to the brain. The transcription factor c-Myc in IBI continues to be implicated in numerous studies. This study was conducted with emphasis placed on the underlying mechanism of c-Myc in IBI. Clinical samples were collected from IBI patients. Middle cerebral artery occlusion (MCAO) was induced in mice by inserting a suture from the external carotid artery to the anterior cerebral artery through the internal carotid artery to mechanically block the blood supply at the origin of the middle cerebral artery, and cortical neurons from mice were exposed to oxygen glucose deprivation (OGD) conditions for IBI model in vitro construction. RT-qPCR was performed to determine microRNA-23b (miR-23b) expression. TUNEL staining and Western blot analysis was conducted to detect apoptosis. The regulatory relationship was analyzed by dual-luciferase reporter gene assay. After loss-and gain-of-function assays, triphenyltetrazolium chloride staining was carried out to detect the area of cerebral infarction, after which the spatial memory in mice was evaluated with Morris water maze test. As per our findings, miR-23b was upregulated in the serum of IBI patients and OGD-treated murine primary neurons. Silencing of miR-23b resulted in reduced OGD-induced neuronal apoptosis. miR-23b inversely targeted nuclear factor erythroid 2-related factor 2 (Nrf2) and c-Myc negatively regulated miR-23b expression. Overexpression of c-Myc and inhibition of miR-23b led to reduced neurological scores of infarction area, neuronal apoptosis, shortened platform arrival time and significantly increased the time spent on the platform quadrant and the times of crossing the platform in vivo. Collectively, downregulated miR-23b by c-Myc might alleviate IBI by upregulating Nrf2.

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RETRACTED: Downregulation of microRNA‐23b protects against ischemia‐reperfusion injury via p53 signaling pathway by upregulating MDM4 in rats

Cited by 11 publications

References 26 publications

Novel Signature Genes for Human Left Ventricle Cardiomyopathies Identified by Weighted Co-expression Network Analysis (WGCNA)

Novel Signature Genes for Human Left Ventricle Cardiomyopathies Identified by Weighted Co-expression Network Analysis (WGCNA)

Co-expression network analysis identified novel potential Signature Genes Associated with human left ventricle cardiomyopathies arises from different etiologies

Downregulation of miR-23b by transcription factor c-Myc alleviates ischemic brain injury by upregulating Nrf2

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