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  • 1
    Online Resource
    Online Resource
    Mapping current research and identifying hotspots of ferroptosis in cardiovascular diseases
    Frontiers Media SA ; 2022
    In:  Frontiers in Cardiovascular Medicine Vol. 9 ( 2022-11-4)
    Details
    In: Frontiers in Cardiovascular Medicine, Frontiers Media SA, Vol. 9 ( 2022-11-4)
    Abstract: Ferroptosis is a unique cell death depended on iron metabolism disorder which is different from previous apoptosis-regulated cell death. Early studies have proposed that ferroptosis is closely associated with multiple cardiovascular diseases (CVDs). However, the relationship of ferroptosis and CVDs has not been summarized by using bibliometric analysis. We intended to illustrate the development of ferroptosis in CVDs over the past years and provide relevant valuable information. Materials and methods The authoritative database of Web of Science Core Collection was collected for retrieving ferroptosis studies in CVDs. In this work, statistical and visualization analysis were conducted using VOSviewer and Citespace. Results A total of 263 studies were included in the final study. From the perspective of the overall literature, the study maintains an increased trend year by year and most manuscripts belonged to original article. China was the most productive country with the utmost scientific research output, as well as the institutions and authors, followed by Germany and the United States of America (USA). Jun Peng from China contributes to the most publications. Collaborative efforts between institutes and authors were limited and there was little widespread cooperation. In addition, burst keywords analysis discovered that ischemia-reperfusion (I/R) injury, heart failure (HF), and atherosclerosis were the top three research directions of ferroptosis in CVDs. The burst investigation and timeline views also indicated that endothelial injury and gut microbiota may also serve as new research topics in the future. Conclusion This study provided comprehensive and specific information about the most influential articles on ferroptosis in CVDs. The relationship between ferroptosis and CVDs had attracted the scholar’s concerns especially in China. Cooperations and communications between countries and institutions should be emphasized and future directions can be concentrated on endothelial disorder and gut microbiota.
    Type of Medium: Online Resource
    ISSN: 2297-055X
    URL: Article
    DOI: 10.3389/fcvm.2022.1046377
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2781496-8
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  • 2
    Online Resource
    Online Resource
    Osteocrin, a novel myokine, prevents diabetic cardiomyopathy via restoring proteasomal activity
    Springer Science and Business Media LLC ; 2021
    In:  Cell Death & Disease Vol. 12, No. 7 ( 2021-06-16)
    Details
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 12, No. 7 ( 2021-06-16)
    Abstract: Proteasomal activity is compromised in diabetic hearts that contributes to proteotoxic stresses and cardiac dysfunction. Osteocrin (OSTN) acts as a novel exercise-responsive myokine and is implicated in various cardiac diseases. Herein, we aim to investigate the role and underlying molecular basis of OSTN in diabetic cardiomyopathy (DCM). Mice received a single intravenous injection of the cardiotrophic adeno-associated virus serotype 9 to overexpress OSTN in the heart and then were exposed to intraperitoneal injections of streptozotocin (STZ, 50 mg/kg) for consecutive 5 days to generate diabetic models. Neonatal rat cardiomyocytes were isolated and stimulated with high glucose to verify the role of OSTN in vitro. OSTN expression was reduced by protein kinase B/forkhead box O1 dephosphorylation in diabetic hearts, while its overexpression significantly attenuated cardiac injury and dysfunction in mice with STZ treatment. Besides, OSTN incubation prevented, whereas OSTN silence aggravated cardiomyocyte apoptosis and injury upon hyperglycemic stimulation in vitro. Mechanistically, OSTN treatment restored protein kinase G (PKG)-dependent proteasomal function, and PKG or proteasome inhibition abrogated the protective effects of OSTN in vivo and in vitro. Furthermore, OSTN replenishment was sufficient to prevent the progression of pre-established DCM and had synergistic cardioprotection with sildenafil. OSTN protects against DCM via restoring PKG-dependent proteasomal activity and it is a promising therapeutic target to treat DCM.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    URL: Article
    DOI: 10.1038/s41419-021-03922-2
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2541626-1
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  • 3
    Online Resource
    Online Resource
    Tisp40 prevents cardiac ischemia/reperfusion injury through the hexosamine biosynthetic pathway in male mice
    Springer Science and Business Media LLC ; 2023
    In:  Nature Communications Vol. 14, No. 1 ( 2023-06-08)
    Details
    In: Nature Communications, Springer Science and Business Media LLC, Vol. 14, No. 1 ( 2023-06-08)
    Abstract: The hexosamine biosynthetic pathway (HBP) produces uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) to facilitate O-linked GlcNAc (O-GlcNAc) protein modifications, and subsequently enhance cell survival under lethal stresses. Transcript induced in spermiogenesis 40 (Tisp40) is an endoplasmic reticulum membrane-resident transcription factor and plays critical roles in cell homeostasis. Here, we show that Tisp40 expression, cleavage and nuclear accumulation are increased by cardiac ischemia/reperfusion (I/R) injury. Global Tisp40 deficiency exacerbates, whereas cardiomyocyte-restricted Tisp40 overexpression ameliorates I/R-induced oxidative stress, apoptosis and acute cardiac injury, and modulates cardiac remodeling and dysfunction following long-term observations in male mice. In addition, overexpression of nuclear Tisp40 is sufficient to attenuate cardiac I/R injury in vivo and in vitro. Mechanistic studies indicate that Tisp40 directly binds to a conserved unfolded protein response element (UPRE) of the glutamine-fructose-6-phosphate transaminase 1 (GFPT1) promoter, and subsequently potentiates HBP flux and O-GlcNAc protein modifications. Moreover, we find that I/R-induced upregulation, cleavage and nuclear accumulation of Tisp40 in the heart are mediated by endoplasmic reticulum stress. Our findings identify Tisp40 as a cardiomyocyte-enriched UPR-associated transcription factor, and targeting Tisp40 may develop effective approaches to mitigate cardiac I/R injury.
    Type of Medium: Online Resource
    ISSN: 2041-1723
    URL: Article
    DOI: 10.1038/s41467-023-39159-0
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2553671-0
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  • 4
    Online Resource
    Online Resource
    Cellular Senescence in Cardiovascular Diseases: A Systematic Review
    Aging and Disease ; 2022
    In:  Aging and disease Vol. 13, No. 1 ( 2022), p. 103-
    Details
    In: Aging and disease, Aging and Disease, Vol. 13, No. 1 ( 2022), p. 103-
    Type of Medium: Online Resource
    ISSN: 2152-5250
    URL: Article
    DOI: 10.14336/AD.2021.0927
    Language: English
    Publisher: Aging and Disease
    Publication Date: 2022
    detail.hit.zdb_id: 2625789-0
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  • 5
    Online Resource
    Online Resource
    A brief overview about the adipokine: Isthmin-1
    Frontiers Media SA ; 2022
    In:  Frontiers in Cardiovascular Medicine Vol. 9 ( 2022-7-26)
    Details
    In: Frontiers in Cardiovascular Medicine, Frontiers Media SA, Vol. 9 ( 2022-7-26)
    Abstract: Isthmin-1 is a secreted protein with multiple capability; however, it truly attracts our attention since the definition as an adipokine in 2021, which exerts indispensable roles in various pathophysiological processes through the endocrine or autocrine manners. In this review, we summarize recent knowledge of isthmin-1, including its distribution, structure, receptor and potential function.
    Type of Medium: Online Resource
    ISSN: 2297-055X
    URL: Article
    DOI: 10.3389/fcvm.2022.939757
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2781496-8
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  • 6
    Online Resource
    Online Resource
    Fibronectin type III domain‐containing 5 improves aging‐related cardiac dysfunction in mice
    Wiley ; 2022
    In:  Aging Cell Vol. 21, No. 3 ( 2022-03)
    Details
    In: Aging Cell, Wiley, Vol. 21, No. 3 ( 2022-03)
    Abstract: Aging is an important risk factor for cardiovascular diseases, and aging‐related cardiac dysfunction serves as a major determinant of morbidity and mortality in elderly populations. Our previous study has identified fibronectin type III domain‐containing 5 (FNDC5) and its cleaved form, irisin, as the cardioprotectant against doxorubicin‐induced cardiomyopathy. Herein, aging or matched young mice were overexpressed with FNDC5 by adeno‐associated virus serotype 9 (AAV9) vectors, or subcutaneously infused with irisin to uncover the role of FNDC5 in aging‐related cardiac dysfunction. To verify the involvement of nucleotide‐binding oligomerization domain‐like receptor with a pyrin domain 3 (NLRP3) and AMP‐activated protein kinase α (AMPKα), Nlrp3 or Ampkα2  global knockout mice were used. Besides, young mice were injected with AAV9‐FNDC5 and maintained for 12 months to determine the preventive effect of FNDC5. Moreover, neonatal rat cardiomyocytes were stimulated with tumor necrosis factor‐α (TNF‐α) to examine the role of FNDC5 in vitro . We found that FNDC5 was downregulated in aging hearts. Cardiac‐specific overexpression of FNDC5 or irisin infusion significantly suppressed NLRP3 inflammasome and cardiac inflammation, thereby attenuating aging‐related cardiac remodeling and dysfunction. In addition, irisin treatment also inhibited cellular senescence in TNF‐α‐stimulated cardiomyocytes in vitro . Mechanistically, FNDC5 activated AMPKα through blocking the lysosomal degradation of glucagon‐like peptide‐1 receptor. More importantly, FNDC5 gene transfer in early life could delay the onset of cardiac dysfunction during aging process. We prove that FNDC5 improves aging‐related cardiac dysfunction by activating AMPKα, and it might be a promising therapeutic target to support cardiovascular health in elderly populations.
    Type of Medium: Online Resource
    ISSN: 1474-9718 , 1474-9726
    URL: Issue
    URL: Article
    DOI: 10.1111/acel.v21.3
    DOI: 10.1111/acel.13556
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2099130-7
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    IRX2 regulates angiotensin II-induced cardiac fibrosis by transcriptionally activating EGR1 in male mice
    Springer Science and Business Media LLC ; 2023
    In:  Nature Communications Vol. 14, No. 1 ( 2023-08-16)
    Details
    In: Nature Communications, Springer Science and Business Media LLC, Vol. 14, No. 1 ( 2023-08-16)
    Abstract: Cardiac fibrosis is a common feature of chronic heart failure. Iroquois homeobox (IRX) family of transcription factors plays important roles in heart development; however, the role of IRX2 in cardiac fibrosis has not been clarified. Here we report that IRX2 expression is significantly upregulated in the fibrotic hearts. Increased IRX2 expression is mainly derived from cardiac fibroblast (CF) during the angiotensin II (Ang II)-induced fibrotic response. Using two CF-specific Irx2 -knockout mouse models, we show that deletion of Irx2 in CFs protect against pathological fibrotic remodelling and improve cardiac function in male mice. In contrast, Irx2 gain of function in CFs exaggerate fibrotic remodelling. Mechanistically, we find that IRX2 directly binds to the promoter of the early growth response factor 1 (EGR1) and subsequently initiates the transcription of several fibrosis-related genes. Our study provides evidence that IRX2 regulates the EGR1 pathway upon Ang II stimulation and drives cardiac fibrosis.
    Type of Medium: Online Resource
    ISSN: 2041-1723
    URL: Article
    DOI: 10.1038/s41467-023-40639-6
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2553671-0
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