通讯机构：
[Chen, Linxi; Li, Lanfang] I;Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, 421001, China. Electronic address:
作者机构：
[Kai Zhang; Lanfang Li] Institute of Pharmacy and Pharmacology , Learning Key Laboratory for Pharmacoproteomics, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang 421001, China;[Nian Fu] Department of Gastroenterology , Affiliated Nanhua Hospital, University of South China, Hengyang Hunan, China;[Li Wang] Institute of Pharmacy and Pharmacology , Learning Key Laboratory for Pharmacoproteomics, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang 421001, China<&wdkj&>Department of Gastroenterology , Affiliated Nanhua Hospital, University of South China, Hengyang Hunan, China
通讯机构：
[Nian Fu] D;[Lanfang Li] I;Institute of Pharmacy and Pharmacology , Learning Key Laboratory for Pharmacoproteomics, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang 421001, China<&wdkj&>Department of Gastroenterology , Affiliated Nanhua Hospital, University of South China, Hengyang Hunan, China
关键词：
cell proliferation;cytoplasm;mitochondria
摘要：
Mitochondrial calcium uniporter (MCU) is a highly selective Ca~(2+) channel protein of the mitochondria inner membrane [1], which allows divalent cations (Ca~(2+) ≈Sr~(2+) >>Mn~(2+) ≈Ba~(2+)) to permeate [2]. The MCU is a 40-kDa protein that contains a proteolytically cleaved mitochondrial import sequence, two coiled-coil domains, two transmembrane domains, and a short motif of amino acids between the two transmembrane domains critical for Ca~(2+) transport [3]. MCU is widely expressed in the mitochondrial inner membrane of various cells [4]. In addition, MCU is also a highly conserved protein among different species (Fig. 1A), suggesting that MCU may play an essential role in the process of physiology and pathology.
作者机构：
[Yangt Yiyuan; Wangt Li; Li Lanfang; Chen Linxi] Institute of Pharmacy and Pharmacology, Learning Key Laboratory for Pharmacoproteomic, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang 421001, China
通讯机构：
[Linxi Chen; Lanfang Li] I;Institute of Pharmacy and Pharmacology, Learning Key Laboratory for Pharmacoproteomic, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China , Hengyang 421001, China
关键词：
nervous system disorders;mitochondria;membrane proteins
摘要：
Connexins and pannexins are two kinds of transmembrane proteins, which play important physiological roles. Connexins form hemichannels and channels, mainly contributing to the formation of gap junctions. Pannexins are newly discovered gap junction proteins and their structures consist of intracellular N-termini, intracellular C termini, an intracellular loop, two extracellular loops, and four transmembrane regions [1]. Because the extracellular domains of pannexins contain glycosylated asparagine residues, pannexins cannot form intercellular channels [2], but in the plasma membrane they can form large pores that can be permeated by ions and other molecules such as ATP [3].
作者机构：
[Li, Lanfang; Zhang, Kai; Chen, Linxi] Univ South China, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Inst Pharm & Pharmacol, Learning Key Lab Pharmacoprote, Hengyang 421001, Peoples R China.;[Cao, Jiangang] Univ South China, Affiliated Nanhua Hosp, Clin Res Inst, Hengyang 421002, Peoples R China.;[He, Lu] Univ South China, Affiliated Hosp 1, Dept Neurosurg, Hengyang 421001, Peoples R China.;[Zhang, Zidong] St Louis Univ, Coll Publ Hlth & Social Justice, St Louis, MO 63103 USA.
通讯机构：
[Li, Lanfang] U;Univ South China, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Inst Pharm & Pharmacol, Learning Key Lab Pharmacoprote, Hengyang 421001, Peoples R China.
关键词：
Cancer;Cardioprotection;FAT10;FAT10ylation;Protein degradation;Ubiquitin-like protein
摘要：
As a member of the ubiquitin-like protein family, the human leukocyte antigen F locus adjacent transcript 10 is composed of two ubiquitin-like domains that have high homology with ubiquitin. Studies have shown that abnormal FAT10 expression and FAT10ylation are crucial to many aspects of cellular biology, such as protein degradation, immune response, regulation of apoptosis and cell cycle progression. In this manuscript, we review some important biological roles of FAT10 in cardioprotection and tumor promotion. FAT10 may be cardioprotective in ischemia and hypoxia through attenuation of hypoxia-induced cardiomyocyte apoptosis regulated by the BCL2/BAX ratio and caveolin-3. In addition, FAT10 may be a novel cancer biomarker that contributes to proliferation, invasion, and metastasis in a broad spectrum of cancer cells, including hepatocellular carcinoma (HCC), glioma, and gastric carcinoma. These findings imply that FAT10 will be a candidate target during treatment of cardiovascular conditions due to its cardioprotective effect. Moreover, FAT10 is a potential therapeutic target in cancer.
通讯机构：
[Chen, LX; Li, LF] U;Univ South China, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Learning Key Lab Pharmacoprote, Inst Pharm & Pharmacol, Hengyang 421001, Peoples R China.
关键词：
Berberine;Cardiovascular diseases;Endoplasmic reticulum stress;Ischemia reperfusion injury;Schisandrin B;Unfolded protein response
摘要：
Endoplasmic reticulum (ER) is an intracellular membranous organelle involved in the synthesis, folding, maturation and post-translation modification of secretory and transmembrane proteins. Therefore, ER is closely related to the maintenance of intracellular homeostasis and the good balance between health and diseases. Endoplasmic reticulum stress (ERS) occurs when unfolded/misfolded proteins accumulate after disturbance of ER environment. In response to ERS, cells trigger an adaptive response called the Unfolded protein response (UPR), which helps cells cope with the stress. In recent years, a large number of studies show that ERS can aggravate cardiovascular diseases. ERS-related proteins expression in cardiovascular diseases is on the rise. Therefore, down-regulation of ERS is critical for alleviating symptoms of cardiovascular diseases, which may be used in the near future to treat cardiovascular diseases. This article reviews the relationship between ERS and cardiovascular diseases and drugs that inhibit ERS. Furthermore, we detail the role of ERS inhibitors in the treatment of cardiovascular disease. Drugs that inhibit ERS are considered as promising strategies for the treatment of cardiovascular diseases.
作者机构：
[Yiyuan Yang; Lanfang Li; Kai Zhang; Linxi Chen] Institute of Pharmacy and Pharmacology, Learning Key Laboratory for Pharmacoproteomics, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, China
通讯机构：
[Linxi Chen; Lanfang Li] I;Institute of Pharmacy and Pharmacology, Learning Key Laboratory for Pharmacoproteomics, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, China
摘要：
Cardiomyocytes, also known as myocardial fibers, are the muscle cells which form the heart tissue. Previous studies have indicated that fetal mammalian cardiomyocytes maintain the regeneration capacity, which promotes the fetal heart growth. Regardless of environment insults including nutrient deprivation, changes of blood flow, along with mechanical and volume loading [1], embryonic mammalian cardiac muscle cells are also related to robust proliferation response. Similarly, the hearts of 1-day-old neonatal mice could also be fully regenerated after surgical resection of the left ventricular apex or myocardial infarction (MI) [2]. Intriguingly, studies have also shown that certain fish, such as adult zebrafish, or urodele amphibians retain an observable capacity for regeneration [3]. In response to cardiac damage, zebrafish exhibits complete regeneration primarily due to the proliferation of cardiomyocytes. Nevertheless, the mouse heart loses this potential in the first week after birth. Tragically, it has been demonstrated that the adult mammalian cardiomyocyte unable to proliferate (Fig. 1A). Adult heart is considered as a terminally differentiated organ [4] that has limited capacity for cardiomyogenesis. Therefore, patients suffering from cardiovascular failure are unable to repair the heart and survive after MI or other heart diseases. Therefore, finding a feasible approach to stimulate adult mammalian cardiomyocyte proliferation is beneficial for the treatment of MI and other heart diseases.
关键词：
Apelin-13;Cardiomyocytes hypertrophy;Ferritin;Ferritinophagy;Mitochondria iron overload;ROS;sideroflexin1
摘要：
Excess iron accumulation and cardiac oxidative stress have been shown as important mediators of cardiac hypertrophy, whereas it remains largely elusive about the occurrence of mitochondrial iron overload and its significance during cardiac hypertrophy. In the present study, we aim to investigate the role of NCOA4-mediated ferritinophagy and SFXN1-dependent mitochondria iron overload in apelin-13-induced cardiomyocytes hypertrophy. Apelin-13 significantly promotes ferric citrate (FAC)-induced total cellular and mitochondria ion production, as well as mitochondria ROS contents. Mechanistically, apelin-13 effectively induces the expression of SFXN1, a mitochondria iron transporting protein and NCOA4, a cargo receptor of ferritinophagy in dose and time-dependent manner. Conversely, blockade of APJ by F13A abolishes these stimulatory effects. In addition, apelin-13-triggered mitochondria iron overload is reversed by the genetic inhibition of SFXN1 and NCOA4. NCOA4 deficiency via its silencing also interferes with the enhanced expression of SFXN1 evoked by apelin-13. In apelin-13-treated H9c2 cells, the promotion in cell diameter, volume as well as protein contents are obviously suppressed by the knockdown of NCOA4 and SFXN1 with their corresponding siRNAs. Remarkably, the human and murine hypertrophic hearts models, as well as apelin-13-injected mice models, present evident cardiac mitochondrial iron deposition and raised expressions of NCOA4 and SFXN1. Taken together, these results provide experimental evidences that NCOA4-mediated ferritinophagy might be defined as an essential mechanism leading to apelin-13-cardiomyocytes hypertrophy in SFXN1-dependent mitochondria iron overload manners.
通讯机构：
[Li, LF; Chen, LX] U;Univ South China, Inst Pharm & Pharmacol, Hengyang 421001, Peoples R China.
关键词：
The P2X7 receptor;Myocardial ischemia-reperfusion injury;Dilated cardiomyopathy;Autoimmune myocarditis;Atherosclerosis;Diabetic retinopathy
摘要：
The P2X7 purinergic receptor, a calcium permeable cationic channel, is activated by extracellular ATP. Most studies show that P2X7 receptor plays an important role in the nervous system diseases, immune response, osteoporosis and cancer. Mounting evidence indicates that P2X7 receptor is also associated with cardiovascular disease. For example, the P2X7 receptor activated by ATP can attenuate myocardial ischemia-reperfusion injury. By contrast, inhibition of P2X7 receptor decreases arrhythmia after myocardial infarction, prolongs cardiac survival after a long term heart transplant, alleviates the dilated cardiomyopathy and the autoimmune myocarditis process. The P2X7 receptor also mitigates vascular diseases including atherosclerosis, hypertension, thrombosis and diabetic retinopathy. This review focuses on the latest research on the role and therapeutic potential of P2X7 receptor in cardiovascular diseases.
作者：
Qionglin Zhou;Kai Zhang;Yu Guo;Linxi Chen;Lanfang Li
期刊：
生物化学与生物物理学报,2018年50(3):319-321 ISSN：1672-9145
通讯作者：
Linxi Chen<&wdkj&>Lanfang Li
作者机构：
[Zhou Qionglin; Zhang Kai; Guo Yu; Chen Linxi; Li Lanfang] Institute of Pharmacy and Pharmacology, University of South China, Learning Key Laboratory for Pharmacoproteomics;[Zhou Qionglin; Zhang Kai; Guo Yu; Chen Linxi; Li Lanfang] Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang, 421001
通讯机构：
[Linxi Chen; Lanfang Li] I
关键词：
pregnancy;embryologic development
摘要：
Acta Biotheoretica is devoted to the promotion of theoretical biology, encompassing mathematical biology and the philosophy of biology, paying special attention to the methodology of formation of biological theory. Papers on all kind of biological theories are welcome. Interesting subjects include philosophy of biology, biomathematics, computational biology, genetics, ecology and morphology. The process of theory formation can be presented in verbal or mathematical form. Moreover, purely methodological papers can be devoted to the historical origins of the philosophy underlying biological theories and concepts. Papers should contain clear statements of biological assumptions, and where applicable, a justification of their translation into mathematical form and a detailed discussion of the mathematical treatment. The connection to empirical data should be clarified. Acta Biotheoretica also welcomes critical book reviews, short comments on previous papers and short notes directing attention to interesting new theoretical ideas. Coverage in the Journals&commat;Ovid database begins with the first 1997 issue.
摘要：
Apelin, an endogenous ligand for the G protein-coupled receptor APJ, is widely expressed in various organs. Recent research has indicated that the Apelin/APJ system plays an important role in aging. Apelin and APJ receptor expression are down-regulated with increasing age. In murine models, Apelin and APJ knockouts exhibit accelerated senescence whereas Apelin-restoration results in enhanced vigor and rejuvenated behavioral and circadian phenotypes. Furthermore, aged Apelin knockout mice develop progressive impairment of cardiac contractility associated with systolic dysfunction. Apelin is crucial to maintain cardiac contractility in aging. Moreover, the Apelin/APJ system appears to be involved in regulation of renin-angiotensin-aldosterone system (RAAS), apoptosis, inflammation and oxidative stress which promotes aging. Likewise, the Apelin/APJ system regulates autophagy, stem cells and the sirtuin family thus contributing to anti-aging. In this review, we describe the relationship between Apelin/APJ system and aging. We elaborate on the role of the Apelin/APJ system in aging stimulators, aging inhibitors and age-related diseases such as obesity, diabetes and cardiovascular disease. We conclude that Apelin/APJ system might become a novel promising therapeutic target for anti-aging.
作者：
Kai Zhang;Qionglin Zhou;Yu Guo;Linxi Chen;Lanfang Li
期刊：
生物化学与生物物理学报,2018年50(6):618-619 ISSN：1672-9145
通讯作者：
Linxi Chen<&wdkj&>Lanfang Li
作者机构：
[Zhang Kai; Zhou Qionglin; Guo Yu; Chen Linxi; Li Lanfang] Institute of Pharmacy and Pharmacology, University of South China, Learning Key Laboratory for Pharmacoproteomics;[Zhang Kai; Zhou Qionglin; Guo Yu; Chen Linxi; Li Lanfang] Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang, 421001
通讯机构：
[Linxi Chen; Lanfang Li] L
关键词：
线粒体;机能障碍;蜂窝;胃;真核细胞;膜;细胞器;房间
摘要：
Both endoplasmic reticulum (ER) and mitochondria are fundamental organelles that coordinate high-order cell functions. ER is an extensive network of cisternae and microtubules, which stretches from the nuclear envelope to the cell surface in all eukaryotic cells. ER works as the site for protein synthesis and corrects post-translational ‘folding’ of proteins. ER also has the ability to transport proteins to their destination. Moreover, ER acts as a calcium ion (Ca~(2+)) reservoir which can be activated by both electrical and chemical stimulation.
