Cardiac lipid metabolism is fundamental to myocardial energy homeostasis, with fatty acid oxidation (FAO) supplying the majority of ATP in the healthy adult heart. This review synthesizes the core regulatory network governing cardiac lipid metabolism, encompassing lipid droplet dynamics mediated by perilipins (e.g., Plin5, Plin2), fatty acid uptake via CD36, systemic lipid modulation by apolipoproteins (e.g., APOC3), and the central energy-sensing AMPK/PGC-1α/PPARα axis. Dysregulation of this network initiates a self-perpetuating lipotoxic cycle, characterized by the accumulation of toxic lipid intermediates (e.g., diacylglycerols, ceramides), oxidative stress, and inflammatory activation, which serves as a common pathological mechanism across diverse cardiovascular diseases (CVDs), including atherosclerosis, heart failure, diabetic cardiomyopathy, and ischemic injury. Emerging from this mechanistic understanding is a promising landscape of biomarkers-such as specific ceramide species, the ApoB/ApoA-1 ratio, and circulating perilipins-and targeted therapeutic strategies, including APOC3 inhibitors, SGLT2 inhibitors, and Plin5-directed therapies. Future advances will depend on integrating multi-omics technologies and precision medicine approaches to tailor interventions to specific metabolic phenotypes, thereby opening new avenues for the prevention and treatment of CVDs.

Lon peptidase 1 (LONP1), a member of the AAA + family, is essential for maintaining mitochondrial function. Recent studies have revealed that LONP1 serves as a multifunctional enzyme, acting not only as a protease but also as a molecular chaperone, interacting with mitochondrial DNA (mtDNA), and playing roles in mitochondrial dynamics, oxidative stress, cellular respiration, and energy metabolism. LONP1 is evolutionarily highly conserved, and mutations or dysfunctions in LONP1 can lead to diseases. There is growing evidence linking LONP1 to various human diseases, such as tumors, neurodegenerative diseases, and heart diseases. This review discusses the discovery, molecular structure, subcellular localization, tissue distribution, and mitochondrial function of LONP1. Furthermore, it summarizes the associations between LONP1 and tumors, neurodegenerative diseases, and heart diseases, exploring its role in different diseases and potential molecular mechanisms. It also analyzes the regulatory effects of related inhibitors and agonists on LONP1. Considering the pleiotropic effects of LONP1, the study of LONP1 is crucial to understanding the relevant pathophysiological processes and developing strategies to modulate and control these related diseases.

BACKGROUND:LIM domain is considered to be important in mediating protein-protein interactions, and members of the LIM protein family can co-regulate tissue-specific gene expression by interacting with different transcription factors. However, its exact function in vivo remains unclear. Our study demonstrates that the LIM protein family member Lmpt may act as a cofactor that interacts with other transcription factors to regulate cellular functions. METHODS:In this study, we generated Lmpt knockdown Drosophila (Lmpt-KD) using the UAS-Gal4 system. We assessed the lifespan and motility of Lmpt-KD Drosophila and analyzed the expression of muscle-related and metabolism-related genes using qRT-PCR. Additionally, we utilized Western blot and Top-Flash luciferase reporter assay to evaluate the level of the Wnt signaling pathway. RESULTS:Our study revealed that knockdown of the Lmpt gene in Drosophila resulted in a shortened lifespan and reduced motility. We also observed a significant increase in oxidative free radicals in the fly gut. Furthermore, qRT-PCR analysis indicated that knockdown of Lmpt led to decreased expression of muscle-related and metabolism-related genes in Drosophila, suggesting that Lmpt plays a crucial role in maintaining muscle and metabolic functions. Finally, we found that reduction of Lmpt significantly upregulated the expression of Wnt signaling pathway proteins. CONCLUSION:Our results demonstrate that Lmpt is essential for motility and survival in Drosophila and acts as a repressor in Wnt signaling.

LIM domain protein 2, also known as LIM protein FHL2, is a member of the LIM-only family. Due to its LIM domain protein characteristics, FHL2 is capable of interacting with various proteins and plays a crucial role in regulating gene expression, cell growth, and signal transduction in muscle and cardiac tissue. In recent years, mounting evidence has indicated that the FHLs protein family is closely associated with the development and occurrence of human tumors. On the one hand, FHL2 acts as a tumor suppressor by down-regulating in tumor tissue and effectively inhibiting tumor development by limiting cell proliferation. On the other hand, FHL2 serves as an oncoprotein by up-regulating in tumor tissue and binding to multiple transcription factors to suppress cell apoptosis, stimulate cell proliferation and migration, and promote tumor progression. Therefore, FHL2 is considered a double-edged sword in tumors with independent and complex functions. This article reviews the role of FHL2 in tumor occurrence and development, discusses FHL2 interaction with other proteins and transcription factors, and its involvement in multiple cell signaling pathways. Finally, the clinical significance of FHL2 as a potential target in tumor therapy is examined.

Drosophila melanogaster, a classical genetic model organism, is widely used in the field of research on cardiac development and pathophysiological changes. Drosophila Lmpt, a LIM domain protein, is highly homologous to the vertebrate Fhl2. Fhl2 mutations cause heart failure, but the molecular mechanism is still unclear. Firstly, we prepared Lmpt polyclonal antibody and detected the expression of endogenous Lmpt in Drosophila muscle tissue and myocardial tissue, suggested Lmpt may play a role in Drosophila heart tissue. Secondly, We constructed Lmpt knockout drosophila by CRISPR/Cas9 system, the Lmpt knockout homozygous were lethal in embryonic stage, and showed absence and disorder of myocardial cells, indicated that Drosophila Lmpt regulates heart development. Thirdly, we found that the expression of Lmpt was down-regulated in dmef2 knockdown Drosophila. Lastly, Lmpt interacted with Mlp84B. We speculated that Drosophila Lmpt might participate in cardiac development through the dmef2-Lmpt/Mlp84B molecular pathway. This research provides a foundation and points out a new direction for the functional study of Lmpt in heart tissue.

黑腹果蝇作为经典遗传学和分子遗传学模式生物,已经成为研究基因调控器官发育以及各种疾病发生的一个强有力的模型。为了探究Mlp84B在果蝇体内的表达定位及互作蛋白质,首先将含启动子元件的果蝇Mlp84B基因组融合GFP序列克隆至pUAST表达载体中,利用胚胎显微注射技术将构建好的重组质粒注射到果蝇早期受精卵;其次通过杂交获得红眼果蝇,经单果蝇建系、平衡子定位后获得稳定遗传的转基因果蝇;最后通过在果蝇体内检测到GFP的表达,同时经qRT-PCR检测到Mlp84B的表达水平上升,证实转基因果蝇构建成功。GFP定位结果显示,内源Mlp84B在果蝇肌肉系统表达,并且Mlp84B与Act57B在果蝇体内相互作用。实验结果表明,文中构建的UAS-Mlp84B-GFP转基因果蝇可以作为肌肉的标记品系,这为探究肌肉系统形成和稳态奠定了基础。

Sphingosine 1-phosphate (S1P), a metabolite of sphingolipids, is mainly derived from red blood cells (RBCs), platelets and endothelial cells (ECs). It plays important roles in regulating cell survival, vascular integrity and inflammatory responses through its receptors. S1P receptors (S1PRs), including 5 subtypes (S1PR1-5), are G protein-coupled receptors and have been proved to mediate various and complex roles of S1P in atherosclerosis, myocardial infarction (MI) and ischemic stroke by regulating endothelial function and inflammatory response as well as immune cell behavior. This review emphasizes the functions of S1PRs in atherosclerosis and ischemic diseases such as MI and ischemic stroke, enabling mechanistic studies and new S1PRs targeted therapies in atherosclerosis and ischemia in the future.

Drosophila melanogaster has been used as a model organism for study on development and pathophysiology of the heart. LIM domain proteins act as adaptors or scaffolds to promote the assembly of multimeric protein complexes. We found a total of 75 proteins encoded by 36 genes have LIM domain in Drosophila melanogaster by the tools of SMART, FLY-FISH, and FlyExpress, and around 41.7% proteins with LIM domain locate in lymph glands, muscles system, and circulatory system. Furthermore, we summarized functions of different LIM domain proteins in the development and physiology of fly heart and hematopoietic systems. It would be attractive to determine whether it exists a probable “LIM code” for the cycle of different cell fates in cardiac and hematopoietic tissues. Next, we aspired to propose a new research direction that the LIM domain proteins may play an important role in fly cardiac and hematopoietic morphogenesis.

<span id="ChDivSummary" name="ChDivSummary" class="abstract-text">目的探讨褪黑素（melatonin,MLT）对胰岛素抵抗（insulin resistance,IR）肝HepG2细胞葡萄糖内生的影响及其机制。方法 HepG2 IR细胞模型采用高糖(25 mmol·L^-1)联合高胰岛素(1μmol·L^-1)培养诱导建立。MLT (10 nmol·L^-1)处理模型细胞6 h后检测糖消耗及糖原含量,GSK-3β、Akt和FoxO1蛋白磷酸化水平检测采用Western blot,免疫荧光法检测FoxO1蛋白核外排情况。结果 IR HepG2细胞经MLT处理后,葡萄糖的摄取和糖原合成增加,p-GSK-3β和p-Akt蛋白水平分别增高约66%和48%,FoxO1磷酸化水平明显提高且细胞质含量增加。结论 MLT可能通过Akt/GSK-3β及Akt/FoxO1信号通路促进胰岛素抵抗HepG2细胞的糖原合成和抑制糖异生,从而改善糖代谢。</span>

叉头框蛋白1(FoxO1)是机体内重要的转录因子,调控着多种基因的表达,它也是胰岛素通路中的关键因子.研究表明FoxO1通过参与胰岛素抵抗、胰岛β细胞增殖分化和凋亡、肥胖相关而在2型糖尿病(T2DM)的发生发展中发挥重要作用.本文就FoxO1对T2DM的影响做简要综述.

Aim To explore the effect of Neu-P11,a novel melatonin agonist with similar function of melatonin,on IOP of acute high IOP animals and the related mechanism.Methods The experiment used the Trendelenburg position(head low feet high position of 80°)to establish acute high IOP model.Rats were placed in the Trendelenburg position and used Tonopen XL contact tonometer to measure IOP(every 5 minutes measured once IOP,and the maximum value in 20 minutes)in 8 :00～9 :00 am.And then,thirty Sprague-Dawley rats(8 week-old)were divided into five groups: normal IOP+normal saline,high IOP+normal saline,high IOP+10 mg·kg-1 Mel,high IOP+20 mg·kg-1 Neu-P11,high IOP+50 mg·kg-1 Neu-P11.Put in a flat to rest 2 h,animals were placed in Trendelenburg position again and then,IOP was measured every hour in the flat by 6 hours.After excessive sodium pentobarbital administration continuous for 1 week,the serum was collected and stored for subsequent detection at the end of the experiment.The level of MDA,SOD and GSH-Px enzyme activity of the rat serum was tested by kit accordingly.HE staining method was used to identify the SD rat retinal morphological changes.Results Trendelenburg position could induce IOP of model group rats,which was increased by 202.9％(P<0.01)and the content of MDA,reduced the activity of SOD and GSH-Px enzyme,retinal thickening was observed and its level was not clear.Neu-P11/Mel could significantly improve oxidative stress level and retinal edema in rats.Conclusion Neu-P11 could reduce IOP of the acute high IOP animals,which might be involved in the lower level of oxidative stress in the body.

<span id="ChDivSummary" name="ChDivSummary" class="abstract-text">&lt;正&gt;水通道蛋白4（aquaporin4,AQP4）是视网膜上重要的水通道蛋白之一,参与房水的分泌和排出,有调节眼内水、电解质运输平衡的功能^[1]。褪黑素（melatonin,Mel）是松果体合成分泌的一种吲哚类神经内分泌激素,可以作为黄斑变性、青光眼以及心血管疾病的一种辅助治疗药物,具有降低眼内压（intraocular pressure,IOP）的作用^[2-3]。然而,褪黑素药</span>

生物技术的飞猛发展及其广泛应用急需创新型人才。生物技术专业的实践操作能力较强，然而现有的实践教学影响了该专业创新型人才的培养，有必要在理论课外补充的前提下，分别从增设综合性实验、设计性实验、TBL实验教学方法及加强实验室管理方面进行改革。通过以上几方面的实施，为适应社会经济发展新常态、输送生物技术专业创新型人才奠定了基础。

Melatonin is biosynthesized in the pineal gland and secreted into the bloodstream. Evidences indicate a role of melatonin in the regulation of glucose metabolism. The objective of this study was to investigate the effect of melatonin on insulin sensitivity in insulin resistant adipocytes. Following a preincubation with melatonin or vehicle for 30 min, insulin resistant cells of 3T3-L1 adipocytes were induced by palmitic acids (300 μM, 6 h). Our results showed that palmitic acids inhibited both the basal and insulin-stimulated uptake of [(3)H]-2-Deoxyglucose, down-regulated the levels of IRS-1 and GLUT-4. However, compared to the vehicle group, melatonin pre-treatment increased significantly the uptake of [(3)H]-2-Deoxyglucose as well as the level of GLUT-4, and decreased phosphorylated IRS-1 (Ser307) although total IRS-1 did not change significantly. These data suggest that palmitic acids impair insulin signal via down-regulating the expressions of IRS-1 and GLUT-4; whereas melatonin can ameliorate insulin sensitivity by inhibiting Ser307 phosphorylation in IRS-1 and increasing GLUT-4 expressions in insulin resistant 3T3-L1 adipocytes. We conclude that melatonin regulates the insulin sensitivity and glucose homeostasis via inhibiting Ser-phosphorylation and improving function of IRS-1.

Melatonin is synthesized and secreted mainly by the pineal gland in a circadian fashion, and it thus mediates endogenous circadian rhythms and influences other physiological functions. Both the G-protein coupled receptors MT1 (encoded by MTNR1A) and MT2 (encoded by MTNR1B) in mammals mediate the actions of melatonin. Evidence from in vivo and in vitro studies proved a key role of melatonin in the regulation of glucose metabolism and the pathogenesis of diabetes, as further confirmed by the recent studies of human genetic variants of MTNR1B. Remarkably, it was also suggested that genetic variations within MTNR1B disordered β-cells function directly, i.e. insulin secretion. This indicated the functional link between MT2 and T2D risk at the protein level, and it may represent the prevailing pathomechanism for how impaired melatonin signaling causes metabolic disorders and increases the T2D risk. It is speculated that melatonin and its receptors may be a new therapeutic avenue in diabetes.

合作学习策略是一种有效的教学组织形式，同时也是培养学生价值取向的一种手段。文章在合作学习内涵的基础上结合南华大学学生的实际，着重探讨了利用合作学习在分子生物学教学中保证有效性的几个因素。

Aim To investigate the effect of Neu-P11,a novel melatonin receptor agonist,on insulin sensitivity in sleep restricted rats as well as the underlying mechanism. Methods Method of rotating cage was adopted to establish SD rat models of sleep restriction. During the 8 days of sleep restriction,rats were injected intraperitoneally with Neu-P11(20 mg /kg),MLT(5 mg /kg),saline respectively every day. Plasma glucose,fasting insulin,malondialdehyde(MDA) levels and enzyme activity of glutathione peroxidase(GSH-Px),superoxide dismutase(SOD) were detected at the end of experiment,the proteins of JNK and phosphorylated JNK in muscles were measured by Western blot. Results Compared with control group,sleep restricted rats showed increased levels of plasma glucose,fasting insulin,but antioxidative potency decreased. However,in Neu-P11 and melatonin-treated sleep restricted rats,the levels of plasma glucose,fasting insulin and MDA decreased with an increase of SOD,GSH-Px activities. Neu-P11 or melatonin also down-regulated the levels of JNK and phosphorylated JNK which were increased by sleep restriction. These data suggest that glucose homeostasis and antioxidative potency of the chronic sleep restricted rats were protected by Neu-P11 and melatonin. Conclusions Neu-P11 could improve metabolic profiles and insulin resistant induced by sleep restriction,and the regulation of JNK and antioxidative potency may be the underlying mechanism.

目的 探讨褪黑素(MLT)对胰岛素抵抗(IR) HepG2细胞葡萄糖代谢的影响及机制. 方法 培养HepG2细胞,高糖高胰岛素(25 mmol/L葡萄糖、1μmol/L胰岛素)诱导24h,建立IR细胞模型并给予MLT(1 nmol/L,10 nmol/L)处理.葡萄糖氧化酶法、蒽酮法和荧光探针法检测HepG2细胞的糖摄取、糖原含量及活性氧(ROS)产率. 结果 HGI孵育HepG2细胞24 h后,细胞的葡萄糖摄取及糖原含量明显减少(P＜0.01),ROS产率显著增加(P＜0.01);而MLT处理增加了IR细胞葡糖糖的摄取(P＜0.01)和糖原合成(P＜0.05),降低ROS的水平(P＜0.01). 结论 MLT可能通过抑制ROS的生成而改善氧化应激,从而促进胰岛素抵抗HepG2细胞葡萄糖的摄取和利用、增强其胰岛素敏感性.

随着生物技术产业经济的发展，对生物技术专业人才的要求日益严格，传统的生物技术专业人才很难满足当今日新月异的经济发展要求。目前，传统的生物技术人才培养，存在着人才知识掌握虽然扎实丰富，但是却缺乏解决实际问题的弊端。如何提高生物技术专业人才的素质，创新一种新的培养方式，是我们应该思考的问题。医学专业由于具有注重实践培训的特点，其培养的人才普遍具有较强的动手能力，在实际问题中能够更好的利用所学的知识去解决问题。所以在生物技术人才培养中，我们可以有效借鉴医学培养的特色，努力的培养出具有专业知识和实践能力的实用型生物技术人才。