Global Research Trends on Ventricular Remodeling: A Bibliometric Analysis From 2012 to 2022

Meng, Tiantian; Wang, Peng; Ding, Jingyi; Du, Ruolin; Gao, Jing; Li, Anqi; Yu, Shanshan; Liu, Jin; Lu, Xinyu; He, Qingyong

doi:10.1016/j.cpcardiol.2022.101332

Cited by 16 publications

(13 citation statements)

References 80 publications

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“…As to the 2022 network, we identified 17 clusters in total and observed the presence of several additional clusters on “myofibroblast”, #0 ( N = 71; S = 0.715; Y = 2018) ( 67 ), on “leukocyte”, #2 ( N = 46; S = 0.877; Y = 2019) ( 6 ), on “mitral valve prolapse”, #4 ( N = 43; S = 0.938; Y = 2018) ( 68 ), on “car-t cells”, #5 ( N = 35; S = 0.935; Y = 1990) ( 69 ), on “systems biology”, #6 ( N = 33; S = 0.92; Y = 2018) ( 70 ), on “apoptosis”, #9 ( N = 24; S = 0.878; Y = 2019) ( 71 ), on “vascular endothelial function”, #10 ( N = 18; S = 0.957; Y = 2018) ( 72 ), on “mitogen-activated protein kinase kinase kinase 3”, #11 ( N = 6; S = 0.993; Y = 2019) ( 73 ), on “extracellular matrix”, #12 ( N = 6; S = 0.988; Y = 2020) ( 74 ), and on “nrg-1”, #17 ( N = 3; S = 1; Y = 2019) ( 75 ), implying an up-to-date trend towards precise identification of specific cellular components and molecular signals closely involved in the initiation and maintenance of cardiac fibrotic events, which may be favorable to tackling cardiac fibrosis as well as its concomitant complicated situations and creating targeted therapies.…”

Section: Resultsmentioning

confidence: 99%

Trends in worldwide research on cardiac fibrosis over the period 1989–2022: a bibliometric study

Mao

Feng

et al. 2023

Front. Cardiovasc. Med.

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BackgroundCardiac fibrosis is a hallmark of various end-stage cardiovascular diseases (CVDs) and a potent contributor to adverse cardiovascular events. During the past decades, extensive publications on this topic have emerged worldwide, while a bibliometric analysis of the current status and research trends is still lacking.MethodsWe retrieved relevant 13,446 articles on cardiac fibrosis published between 1989 and 2022 from the Web of Science Core Collection (WoSCC). Bibliometrix was used for science mapping of the literature, while VOSviewer and CiteSpace were applied to visualize co-authorship, co-citation, co-occurrence, and bibliographic coupling networks.ResultsWe identified four major research trends: (1) pathophysiological mechanisms; (2) treatment strategies; (3) cardiac fibrosis and related CVDs; (4) early diagnostic methods. The most recent and important research themes such as left ventricular dysfunction, transgenic mice, and matrix metalloproteinase were generated by burst analysis of keywords. The reference with the most citations was a contemporary review summarizing the role of cardiac fibroblasts and fibrogenic molecules in promoting fibrogenesis following myocardial injury. The top 3 most influential countries were the United States, China, and Germany, while the most cited institution was Shanghai Jiao Tong University, followed by Nanjing Medical University and Capital Medical University.ConclusionsThe number and impact of global publications on cardiac fibrosis has expanded rapidly over the past 30 years. These results are in favor of paving the way for future research on the pathogenesis, diagnosis, and treatment of cardiac fibrosis.

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Section: Resultsmentioning

confidence: 99%

Trends in worldwide research on cardiac fibrosis over the period 1989–2022: a bibliometric study

Mao

Feng

et al. 2023

Front. Cardiovasc. Med.

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“…The mechanism of cardiac remodeling is very complex, which is the result of the comprehensive action of a variety of pathological factors [ 32 , 33 ]. The main factors that promote the development of cardiac remodeling include myocardial fibrosis, excessive deposition of extracellular matrix, oxidative stress and apoptosis [ 34 , 35 ]. Up to now, the progress of improving and alleviating cardiac remodeling is still the focus and difficulty in the treatment of cardiovascular disease [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Stomatin-like protein 2 deficiency exacerbates adverse cardiac remodeling

Jiang

et al. 2023

Cell Death Discov.

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Myocardial fibrosis, oxidative stress, and autophagy both play key roles in the progression of adverse cardiac remodeling. Stomatin-like protein 2 (SLP-2) is closely related to mitochondrial function, but little is known about its role and mechanism in cardiac remodeling. We developed doxorubicin (Dox), angiotensin (Ang) II, and myocardial ischemia-reperfusion (I/R) injury induced cardiac remodeling model and Dox treated H9C2 cell injury model using SLP-2 knockout (SLP-2-/-) mice and H9C2 cells with low SLP-2 expression. We first examined cardiac functional and structural changes as well as levels of oxidative stress, apoptosis and autophagy. We found that SLP-2 deficiency leads to decreased cardiac function and promotes myocardial fibrosis. After Dox and Ang II treatment, SLP-2 deficiency further aggravated myocardial fibrosis, increased myocardial oxidative stress and apoptosis, and activated autophagy by inhibiting PI3K-Akt-mTOR signaling pathway, ultimately exacerbating adverse cardiac remodeling. Similarly, SLP-2 deficiency further exacerbates adverse cardiac remodeling after myocardial I/R injury. Moreover, we extracted cardiomyocyte mitochondria for proteomic analysis, suggesting that SLP-2 deficiency may be involved in myocardial I/R injury induced adverse cardiac remodeling by influencing ubiquitination of intramitochondrial proteins. In addition, the oxidative stress, apoptosis and autophagy levels of H9C2 cells with low SLP-2 expression were further enhanced, and the PI3K-Akt-mTOR signaling pathway was further inhibited under Dox stimulation. Our results suggest that SLP-2 deficiency promotes myocardial fibrosis, disrupts normal mitochondrial function, overactivates autophagy via PI3K-Akt-mTOR signaling pathway, affects the level of ubiquitination, leads to irreversible myocardial damage, and ultimately exacerbates adverse cardiac remodeling.

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“…Though considerable progress has been made in the diagnosis and treatment of myocardial infarction (MI), which is still the leading cause of death worldwide [ 1 ], the progression of MI often leads to adverse ventricular remodeling, eventually resulting in ventricular dysfunction and death [ 2 , 3 , 4 ]. The immune system plays a crucial role in the ventricular remodeling process and contributes to both the inflammatory and reparative phases [ 5 , 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

CCR7 Mediates Dendritic-Cell-Derived Exosome Migration and Improves Cardiac Function after Myocardial Infarction

et al. 2023

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Dendritic cells (DCs) play key roles in promoting wound healing after myocardial infarction (MI). Our previous studies have shown that exosomes derived from DCs (DEXs) could migrate to lymphoid tissue and improve cardiac function post-MI by activating CD4+ T cells; however, the mechanism of DEXs’ migration to lymphoid tissue and the improvement of cardiac function are still unknown. In our study, we found that CCR7 expression significantly increased in MI-DEXs compared with control-DEXs; meanwhile, CCL19 and CCL21, the ligands of CCR7, significantly increased in the serum of MI-model mice. Subsequently, we overexpressed and knocked down CCR7 in MI-DEXs and found that overexpressed CCR7 enhanced the migration of MI-DEXs to the spleen; however, CCR7 knockdown attenuated MI-DEXs’ migration according to near-IR fluorescence imaging. Furthermore, overexpressed CCR7 in MI-DEXs enhanced the MI-DEXs’ improvement of cardiac function after MI; however, CCR7-knockdown MI-DEXs attenuated this improvement. In addition, after DEXs’ migration to the spleen, MI-DEXs activated CD4+ T cells and induced the expression of IL-4 and IL-10, which were significantly increased in the MI-DEX group compared with the control group. In conclusion, CCR7 could mediate DEXs’ migration to the spleen and improve cardiac function after MI, and we found that the mechanism was partly via activation of CD4+ T cells and secretion of IL-4 and IL-10. Our study presented an innovative method for improving cardiac function by enhancing the migration ability of MI-DEXs after MI, while CCR7 could be a potential candidate for MI-DEX bioengineering to enhance migration.

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Global Research Trends on Ventricular Remodeling: A Bibliometric Analysis From 2012 to 2022

Cited by 16 publications

References 80 publications

Trends in worldwide research on cardiac fibrosis over the period 1989–2022: a bibliometric study

Trends in worldwide research on cardiac fibrosis over the period 1989–2022: a bibliometric study

Stomatin-like protein 2 deficiency exacerbates adverse cardiac remodeling

CCR7 Mediates Dendritic-Cell-Derived Exosome Migration and Improves Cardiac Function after Myocardial Infarction

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