<i>Period 2</i>-Induced Activation of Autophagy Improves Cardiac Remodeling After Myocardial Infarction

Zhang, Xinyu; Wang, Lin; Yan, Wenjiang; Lu, Xiaoting; Li, Xinyun; Sun, Yuanyuan

doi:10.1089/hum.2019.146

Cited by 7 publications

(3 citation statements)

References 41 publications

(42 reference statements)

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“…24 Another study also revealed that PER2 overexpression facilitated the expression of Beclin1, which was necessary for autophagy and apoptosis. 25 Consequently, PER2 played a crucial role in the process of autophagy and might impact the pathogenesis of SLE through autophagy pathway.…”

Section: Discussionmentioning

confidence: 99%

Association of PER2 gene single nucleotide polymorphisms with genetic susceptibility to systemic lupus erythematosus

Dan

Zhao

Mao

et al. 2021

Lupus

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The circadian clock plays a crucial role in the progress of systemic lupus erythematosus (SLE). In this study, we performed a case-control study to explore the association between Period 2 (PER2) gene single nucleotide polymorphisms (SNPs) and the susceptibility of systemic lupus erythematosus (SLE). A total of 492 SLE patients and 493 healthy controls were included. The improved multiple ligase detection reaction (iMLDR) was used for genotyping. The correlations between four SNPs of PER2 (rs10929273, rs11894491, rs36124720, rs934945) and the genetic susceptibility and clinical manifestations of SLE were analyzed. Significant differences were observed in the distributions of allele frequencies and genotype under dominant model in rs11894491 between SLE patients and controls ( p = 0.030, p = 022, respectively). We hypothesized that PER2 gene SNPs was related to the genetic susceptibility and clinical manifestations, implying the potential role of PER2 in the pathogenesis of SLE.

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Section: Discussionmentioning

confidence: 99%

Association of PER2 gene single nucleotide polymorphisms with genetic susceptibility to systemic lupus erythematosus

Dan

Zhao

Mao

et al. 2021

Lupus

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“…Autophagy is a complex process that involves multiple factors. In mammals, LC3B-I is conjugated with phosphatidylethanolamine to form LC3B-II, resulting in the maturation of autophagosomes [ 40 ]. Dysregulation of autophagy is associated with a number of cardiac diseases, including cardiomyopathy [ 41 ], ischemic heart disease [ 42 ], and heart failure [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

Continuous Infusion of Angiotensin IV Protects against Acute Myocardial Infarction via the Inhibition of Inflammation and Autophagy

Bai

Wang

Chun-hua

et al. 2021

Oxidative Medicine and Cellular Longevity

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Acute myocardial infarction (AMI) is a major cause of morbidity and mortality worldwide. Angiotensin (Ang) IV possesses many biological properties that are not yet completely understood. Therefore, we investigated the function and mechanism of Ang IV in AMI in in vivo and in vitro conditions. AMI was performed by ligation of the left anterior descending coronary artery (LAD) in male C57 mice. Ang IV was continuously infused by a minipump 3 d before AMI for 33 d. The neonatal rat ventricular myocytes (NRVCs) were stimulated with Ang IV and cultured under hypoxic conditions. In vivo, Ang IV infusion significantly reduced the mortality after AMI. By the 7th day after AMI, compared with the AMI group, Ang IV reduced the inflammatory cytokine expression. Moreover, terminal deoxyribonucleotidyl transferase- (TDT-) mediated dUTP nick-end labeling (TUNEL) assay showed that Ang IV infusion reduced AMI-induced cardiomyocyte apoptosis. Compared with AMI, Ang IV reduced autophagosomes in cardiomyocytes and improved mitochondrial swelling and disarrangement, as assessed by transmission electron microscopy. By 30th day after AMI, Ang IV significantly reduced the ratio of heart weight to body weight. Echocardiography showed that Ang IV improved impaired cardiac function. Hematoxylin and eosin (H&E) and Masson staining showed that Ang IV infusion reduced the infarction size and myocardial fibrosis. In vitro, dihydroethidium (DHE) staining and comet assay showed that, compared with the hypoxia group, Ang IV reduced oxidative stress and DNA damage. Enzyme-linked immunosorbent assay (ELISA) showed that Ang IV reduced hypoxia-induced secretion of the tumor necrosis factor- (TNF-) ɑ and interleukin- (IL-) 1β. In addition, compared with the hypoxia group, Ang IV reduced the transformation of light chain 3- (LC3-) I to LC3-II but increased p62 expression and decreased cardiomyocyte apoptosis. Overall, the present study showed that Ang IV reduced the inflammatory response, autophagy, and fibrosis after AMI, leading to reduced infarction size and improved cardiac function. Therefore, administration of Ang IV may be a feasible strategy for the treatment of AMI.

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“…118 Interestingly, endothelial cells of Bmal1 −/− or Per2 −/− mice demonstrate significantly decreased endothelial nitric oxide synthase activation and, consequently, reduced nitric oxide production and increased superoxide levels. 36,119 Furthermore, studies have shown that PER2 overexpression improves cardiac remodeling post-MI, 120 and PER2 is essential to maintain early endothelial progenitor cell function and angiogenesis after MI in mice. 121 In contrast to the above mentioned research, two studies from the same research group found protective effects from MI in the mPer2 mutant mouse model.…”

Section: The Circadian Clockwork Mechanism In the Cardiovascular Systemmentioning

confidence: 99%

Circadian Influences on Myocardial Ischemia-Reperfusion Injury and Heart Failure

Eckle,

Bertazzo,

Khatua

et al. 2024

Circulation Research

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The impact of circadian rhythms on cardiovascular function and disease development is well established, with numerous studies in genetically modified animals emphasizing the circadian molecular clock’s significance in the pathogenesis and pathophysiology of myocardial ischemia and heart failure progression. However, translational preclinical studies targeting the heart's circadian biology are just now emerging and are leading to the development of a novel field of medicine termed circadian medicine. In this review, we explore circadian molecular mechanisms and novel therapies, including (1) intense light, (2) small molecules modulating the circadian mechanism, and (3) chronotherapies such as cardiovascular drugs and meal timings. These promise significant clinical translation in circadian medicine for cardiovascular disease. (4) Additionally, we address the differential functioning of the circadian mechanism in males versus females, emphasizing the consideration of biological sex, gender, and aging in circadian therapies for cardiovascular disease.

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Period 2-Induced Activation of Autophagy Improves Cardiac Remodeling After Myocardial Infarction

Cited by 7 publications

References 41 publications

Association of PER2 gene single nucleotide polymorphisms with genetic susceptibility to systemic lupus erythematosus

Association of PER2 gene single nucleotide polymorphisms with genetic susceptibility to systemic lupus erythematosus

Continuous Infusion of Angiotensin IV Protects against Acute Myocardial Infarction via the Inhibition of Inflammation and Autophagy

Circadian Influences on Myocardial Ischemia-Reperfusion Injury and Heart Failure

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