LncRNAs and Cardiovascular Disease

Hennessy, Elizabeth J.

doi:10.1007/978-3-030-92034-0_5

Cited by 7 publications

(3 citation statements)

References 164 publications

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“…Therefore, the conjugation of lncRNA-silencing elements with nanoparticle drug carriers may lead to macrophage-targeting nanodrug development and contribute to new therapies. It is becoming increasingly clear that lncRNAs function through various mechanisms during the onset and progression of CVDs, such as MI and arrhythmia, cardiac remodeling, and heart failure (46)(47)(48). However, the potential molecular mechanism has not been cleared.…”

Section: Discussionmentioning

confidence: 99%

lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats

Wang

Yin

et al. 2023

Front. Cardiovasc. Med.

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ObjectiveSympathetic remodeling after myocardial infarction (MI) is the primary cause of ventricular arrhythmias (VAs), leading to sudden cardiac death (SCD). M1-type macrophages are closely associated with inflammation and sympathetic remodeling after MI. Long noncoding RNAs (lncRNAs) are critical for the regulation of cardiovascular disease development. Therefore, this study aimed to identify the lncRNAs involved in MI and reveal a possible regulatory mechanism.Methods and resultsM0- and M1-type macrophages were selected for sequencing and screened for differentially expressed lncRNAs. The data revealed that lncRNA LOC100911717 was upregulated in M1-type macrophages but not in M0-type macrophages. In addition, the lncRNA LOC100911717 was upregulated in heart tissues after MI. Furthermore, an RNA pull-down assay revealed that lncRNA LOC100911717 could interact with growth-associated protein 43 (GAP43). Essentially, immunofluorescence assays and programmed electrical stimulation demonstrated that GAP43 expression was suppressed and VA incidence was reduced after lncRNA LOC100911717 knockdown in rat hearts using an adeno-associated virus.ConclusionsWe observed a novel relationship between lncRNA LOC100911717 and GAP43. After MI, lncRNA LOC100911717 was upregulated and GAP43 expression was enhanced, thus increasing the extent of sympathetic remodeling and the frequency of VA events. Consequently, silencing lncRNA LOC100911717 could reduce sympathetic remodeling and VAs.

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Section: Discussionmentioning

confidence: 99%

lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats

Wang

Yin

et al. 2023

Front. Cardiovasc. Med.

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“…LncRNAs are ncRNAs of more than 200 nt, that do not translate proteins, but their regulatory role in mediating cell processes cannot be ignored [ 2 ]. It is widely involved in the development and treatment of diseases, such as tumors, cardiovascular diseases（CVD）, diabetes, and arthritis, etc [ [3] , [4] , [5] , [6] , [7] , [8] ].…”

Section: Introductionmentioning

confidence: 99%

New mechanism of LncRNA: In addition to act as a ceRNA

Zhang,

Zhu,

et al. 2024

Non-coding RNA Research

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“…An increasing number of lncRNAs have been associated with both important biological functions and pathological conditions such as diabetes, neurodegenerative diseases, rheumatoid arthritis, cardiovascular diseases, and cancer (48)(49)(50). Dahariya et al suggest that activation and inhibition of gene expression are promoted by lncRNAs through diverse molecular mechanisms comprising of four basic mechanisms: signal, decoy, guide, and scaffold.…”

Section: Introductionmentioning

confidence: 99%

Emerging role of lncRNAs in drug resistance mechanisms in head and neck squamous cell carcinoma

et al. 2022

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Head and neck squamous cell carcinoma (HNSCC) originates in the squamous cell lining the mucosal surfaces of the head and neck region, including the oral cavity, nasopharynx, tonsils, oropharynx, larynx, and hypopharynx. The heterogeneity, anatomical, and functional characteristics of the patient make the HNSCC a complex and difficult-to-treat disease, leading to a poor survival rate and a decreased quality of life due to the loss of important physiologic functions and aggressive surgical injury. Alteration of driver-oncogenic and tumor-suppressing lncRNAs has recently been recently in HNSCC to obtain possible biomarkers for diagnostic, prognostic, and therapeutic approaches. This review provides current knowledge about the implication of lncRNAs in drug resistance mechanisms in HNSCC. Chemotherapy resistance is a major therapeutic challenge in HNSCC in which lncRNAs are implicated. Lately, it has been shown that lncRNAs involved in autophagy induced by chemotherapy and epithelial–mesenchymal transition (EMT) can act as mechanisms of resistance to anticancer drugs. Conversely, lncRNAs involved in mesenchymal–epithelial transition (MET) are related to chemosensitivity and inhibition of invasiveness of drug-resistant cells. In this regard, long non-coding RNAs (lncRNAs) play a pivotal role in both processes and are important for cancer detection, progression, diagnosis, therapy response, and prognostic values. As the involvement of more lncRNAs is elucidated in chemoresistance mechanisms, an improvement in diagnostic and prognostic tools could promote an advance in targeted and specific therapies in precision oncology.

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LncRNAs and Cardiovascular Disease

Cited by 7 publications

References 164 publications

lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats

lncRNA LOC100911717-targeting GAP43-mediated sympathetic remodeling after myocardial infarction in rats

New mechanism of LncRNA: In addition to act as a ceRNA

Emerging role of lncRNAs in drug resistance mechanisms in head and neck squamous cell carcinoma

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