Corrigendum: Inhibition of TGF-β/Smad3 Signaling Disrupts Cardiomyocyte Cell Cycle Progression and Epithelial–Mesenchymal Transition-Like Response During Ventricle Regeneration

Peng, Yuanyuan; Wang, Wenyuan; Fang, Yunzheng; Hu, Haichen; Chang, Nannan; Pang, Meijun; Hu, Ye-Fan; Li, Xueyu; Long, Han; Xiong, Jing-Wei; Zhang, Ruilin

doi:10.3389/fcell.2021.699796

Cited by 2 publications

(1 citation statement)

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“…The TGF-β/Smad3 signaling pathway has also been implicated in cardiac regeneration. For instance, the inhibition of Smad3 in a model of ventricular ablation in zebrafish reduces CMs proliferation and migration; concretely, the cell cycle is disrupted and EMT response is impaired, limiting cardiac regeneration [ 160 ] ( Figure 3 A). Mukherjee et al (2020) observed in zebrafish that Cellular communication network factor 2a (Ccn2a) is induced in ECs in the injured tissue and regulates CMs proliferation ( Figure 3 A).…”

Section: Reactivation Of Cell Proliferation For Heart Repairmentioning

confidence: 99%

Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart—Part II: Molecular Mechanisms of Cardiac Regeneration

Castillo-Casas,

Caño-Carrillo,

Sánchez-Fernández

et al. 2023

JCDD

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Cardiovascular diseases are the leading cause of death worldwide, among which ischemic heart disease is the most representative. Myocardial infarction results from occlusion of a coronary artery, which leads to an insufficient blood supply to the myocardium. As it is well known, the massive loss of cardiomyocytes cannot be solved due the limited regenerative ability of the adult mammalian hearts. In contrast, some lower vertebrate species can regenerate the heart after an injury; their study has disclosed some of the involved cell types, molecular mechanisms and signaling pathways during the regenerative process. In this ‘two parts’ review, we discuss the current state-of-the-art of the main response to achieve heart regeneration, where several processes are involved and essential for cardiac regeneration.

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Section: Reactivation Of Cell Proliferation For Heart Repairmentioning

confidence: 99%

Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart—Part II: Molecular Mechanisms of Cardiac Regeneration

Castillo-Casas,

Caño-Carrillo,

Sánchez-Fernández

et al. 2023

JCDD

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Adverse effect signature extraction and prediction for drugs treating COVID-19

Wang

et al. 2022

Front. Genet.

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Given the considerable cost of drug discovery, drug repurposing is becoming attractive as it can effectively shorten the development timeline and reduce the development cost. However, most existing drug-repurposing methods omitted the heterogeneous health conditions of different COVID-19 patients. In this study, we evaluated the adverse effect (AE) profiles of 106 COVID-19 drugs. We extracted four AE signatures to characterize the AE distribution of 106 COVID-19 drugs by non-negative matrix factorization (NMF). By integrating the information from four distinct databases (AE, bioassay, chemical structure, and gene expression information), we predicted the AE profiles of 91 drugs with inadequate AE feedback. For each of the drug clusters, discriminant genes accounting for mechanisms of different AE signatures were identified by sparse linear discriminant analysis. Our findings can be divided into three parts. First, drugs abundant with AE-signature 1 (for example, remdesivir) should be taken with caution for patients with poor liver, renal, or cardiac functions, where the functional genes accumulate in the RHO GTPases Activate NADPH Oxidases pathway. Second, drugs featuring AE-signature 2 (for example, hydroxychloroquine) are unsuitable for patients with vascular disorders, with relevant genes enriched in signal transduction pathways. Third, drugs characterized by AE signatures 3 and 4 have relatively mild AEs. Our study showed that NMF and network-based frameworks contribute to more precise drug recommendations.

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Corrigendum: Inhibition of TGF-β/Smad3 Signaling Disrupts Cardiomyocyte Cell Cycle Progression and Epithelial–Mesenchymal Transition-Like Response During Ventricle Regeneration

Cited by 2 publications

References 0 publications

Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart—Part II: Molecular Mechanisms of Cardiac Regeneration

Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart—Part II: Molecular Mechanisms of Cardiac Regeneration

Adverse effect signature extraction and prediction for drugs treating COVID-19

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