细胞生理学和生物化学是一个致力于推进基础细胞研究前沿的多学科科学论坛。它面向来自生理和生化学科以及遗传学、分子生物学、病理生理学、病理生物化学和细胞毒理学和药理学等相关领域的科学家。发表了关于细胞内传递、细胞代谢、细胞生长、分化和死亡、离子通道和载体以及细胞体积的维持、调节和干扰的机制的原创论文和综述。细胞生理学和生物化学每月都会在同行评审下出现，在国际社会共同努力解开细胞功能机制方面发挥了积极作用。

Cellular Physiology and Biochemistry is a multidisciplinary scientific forum dedicated to advancing the frontiers of basic cellular research. It targets scientists from various fields, including physiology, biochemistry, genetics, molecular biology, pathophysiology, pathobiochemistry, cytotoxicology, and pharmacology. The journal publishes original papers and reviews on mechanisms of intracellular signaling, cellular metabolism, growth, differentiation, and death, as well as the maintenance, regulation, and disruption of cell volume, ion channels, and carriers. It is published monthly and undergoes peer review, playing an active role in the international community's efforts to unravel the mechanisms of cellular function.

《Cellular Physiology and Biochemistry》是一个多学科科学论坛，致力于推动基础细胞研究的前沿。该期刊面向来自生理学、生物化学、遗传学、分子生物学、病理生理学、病理生物化学、细胞毒理学和药理学等相关领域的科学家。期刊发表原创论文和综述，内容涵盖细胞内信号传递、细胞代谢、细胞生长、分化与死亡、离子通道和载体的机制，以及细胞体积的维持、调节和干扰等方面。每月定期出版，并经过同行评审，为国际科学界共同揭示细胞功能机制做出了积极贡献。

Cellular Physiology and Biochemistry

Background: Stress fracture is one of the most common overuse injuries in athletes. Overloaded mechanical stimulation is an important factor affecting stress fractures, but the mechanism is unclear. Methods: MC3T3-E1 cells and a polycaprolactone (PCL) scaffold were co-cultured, and finite element analysis (FEA) was used to analyze the load-carrying capability. Cell proliferation was investigated with CCK-8 assays. An alkaline phosphatase (AKP) activity assay was used to evaluate cell differentiation. Cell apoptosis was analyzed using Hoechst/ PI double-labeling, Caspase-3 activity and lactate dehydrogenase (LDH) activity assays. Realtime PCR and Western blotting were used to examine the gene and protein expression, respectively, of Caspase-3 and Caspase-9. Assays of the intracellular calcium with fluorescent probe technique and extracellular ATP with fluorometric assay kit were used to analyze the changes in the intracellular calcium concentration induced by calcium channel opening and the release of ATP, respectively, at different operation times. Results: When the apparent strain reached 10000 µε, the strain scope of fber at levels greater than 4000 µε was 60%. Overloading for 4 days and operation times of 0.5 h and 2 h increased the cell number and AKP secretion. However, apoptosis genes were activated at the same time, and the operation time of 2 h had a significantly greater effect than 0.5 h. At 8 days, the cell numbers were greater for the operation time of 0.5 h than for 2 h, and the 2-h groups had the fastest apoptosis rate. Overloading for 1 day increased intracellular calcium levels and ATP release. The increase in intracellular calcium could be blocked by the addition of N-ethylmaleimide (NEM) or Hank's medium. Overloading for 8 days increased intracellular calcium levels but decreased extracellular ATP, and verapamil blocked the increase in intracellular calcium. Conclusion: We found that a simultaneous ‘double effect’ on osteoblasts was induced by overloading, which promoted cell proliferation, differentiation and apoptosis. Short-term overloading could open the cell membrane calcium channels and release calcium stores to elevate intracellular calcium levels, thereby promoting the proliferation and differentiation of cells to a greater extent than the effect of apoptosis. For long-term overloading, calcium channel opening in the membrane could lead to overloading of intracellular calcium levels, inducing an apoptosis effect that is greater than the effect on proliferation and differentiation.

Lu Liu

Hui Li

Ying Cui

Ruixin Li

Fan Meng

Zi Ye

Xizheng Zhang

Calcium Channel Opening Rather than the Release of ATP Causes the Apoptosis of Osteoblasts Induced by Overloaded Mechanical Stimulation

Oxidative stress and infections by Pseudomonas aeruginosa (P. aeruginosa) are prominent in lungs of patients suffering from cystic fibrosis (CF).The present study examines effects of P. aeruginosa on lipid peroxidation in human and mouse lungs, and cell death induced by P. aeruginosa in human airway epithelial cells. The role of the Ca2+ activated Cl- channel TMEM16A, the phospholipid scramblase TMEM16F, and the CFTR Cl- channel for ferroptotic cell death is examined.Lipid peroxidation was detected in human CF lungs, which correlated with bacterial infection. In vivo inoculation with P. aeruginosa or Staphylococcus aureus (S. aureus) induced lipid peroxidation in lungs of mice lacking expression of CFTR, and in lungs of wild type animals. Incubation of CFBE human airway epithelial cells with P. aeruginosa induced an increase in reactive oxygen species (ROS), causing lipid peroxidation and cell death independent of expression of wt-CFTR or F508del-CFTR. Knockdown of TMEM16A attenuated P. aeruginosa induced cell death. Antioxidants such as coenzyme Q10 and idebenone as well as the inhibitor of ferroptosis, ferrostatin-1, inhibited P. aeruginosa-induced cell death. CFBE cells expressing wtCFTR, but not F508del-CFTR, activated a basal Cl- conductance upon exposure to P. aeruginosa, which was caused by an increase in intracellular basal Ca2+ concentrations and activation of Ca2+-dependent adenylate cyclase.The data suggest an intrinsic pro-inflammatory phenotype in CF epithelial cells, while ferroptosis is observed in both non-CF and CF epithelial cells upon infection with P. aeruginosa. CF cells fail to activate fluid secretion in response to infection with P. aeruginosa. The use of antioxidants and inhibitors of ferroptosis is proposed as a treatment of pneumonia caused by infection with P. aeruginosa.

Jiraporn Ousingsawat

Rainer Schreiber

Erich Gulbins

Markus Kamler

Karl Kunzelmann

P. aeruginosa Induced Lipid Peroxidation Causes Ferroptotic Cell Death in Airways

铜绿假单胞菌诱导的脂质过氧化导致呼吸道铁死亡

Accumulating evidence suggests that atherosclerotic progression depends on persistent and chronic inflammation in the arterial walls. MicroRNA-155 is reportedly involved in cardiovascular disease and has been implicated as a pro-inflammation regulator. Although some researchers have focused on microRNA-155 as an atherosclerosis regulator, the mechanisms by which microRNA-155 functions as a putative pro-atherosclerosis microRNA are largely unknown. This study aims to analyze microRNA-155's effects on atherosclerotic inflammation and to explore its mechanism.MicroRNA-155's effects on atherosclerotic inflammation were observed along with the expression and activity levels of SOCS1, STAT3 and NF-κB though microRNA-155 inhibition or overexpression.Highly expressions of microRNA-155 in oxLDL-stimulated macrophages and atherosclerosis mice were inversely correlated with SOCS1 expression. Ectopic microRNA-155 overexpression significantly promoted inflammatory cytokine and chemokine production and atherosclerosis progression. We then observed microRNA-155's functional role in the atherosclerotic pathophysiological process in vivo and in vitro. The observation revealed that by enhancing STAT3 and NF-κB signaling and facilitating immune inflammation by targeting SOCS1, microRNA-155 plays a promotable role in atherosclerosis progression.microRNA-155 works as a promoter in the atherosclerotic procession. Its mechanism may include enhancing inflammatory response in atherosclerosis by increasing STAT3 and NF-κB signaling via targeting SOCS1.

Yang Yang

Lixia Yang

Xing Liang

Guofu Zhu

MicroRNA-155 Promotes Atherosclerosis Inflammation via Targeting SOCS1

微小RNA-155通过靶向SOCS1促进动脉粥样硬化炎症

Background: MicroRNAs (miRNAs) have emerged as key players in various human biological processes, including tumorigenesis. Here, we investigated the roles of miR-375 in the pathogenesis of oral squamous cell carcinoma (OSCC). Methods: We performed quantitative real-time PCR (qRT-PCR) to detect miR-375 expression in OSCC tissues and corresponding normal oral epithelial tissues and analyze the correlation of miR-375 expression with OSCC metastasis and patient’s survival. Then, the effects of miR-375 expression on proliferation, cell cycle, apoptosis and radiosensitivity in OSCC cells were determined by using MTT, flow cytometry and clonogenic survival assays. A dual-luciferase reporter assay was performed to test whether miR-375 binds to the 3’-untranslated region (3’-UTR) of target mRNA. Results: The expression level of miR-375 in OSCC tissues was significantly lower than that in normal oral epithelial tissues, and low miR-375 expression was correlated with higher incidence of lymph node metastasis and poor survival of OSCC patients. Upregulation of miR-375 significantly inhibits growth, induces cell cycle arrest in G0/G1 phase, increases apoptosis and enhances radiosensitivity in OSCC cells. Analysis of luciferase activity demonstrated that miR-375 binds to the 3’-UTR of insulin like growth factor 1 receptor (IGF-1R). Small interfering RNA (shRNA)-mediated IGF-1R knockdown mimics the effects of miR-375 upregulation, while overexpression of IGF-1R partially reverses those effects in OSCC cells. Conclusion: It was obviously demonstrated that miRNA-375 inhibits growth and enhances radiosensitivity in OSCC cells by targeting IGF-1R, suggesting that miR-375 may be a potential therapeutic target for OSCC patients.

MicroRNA-375 Inhibits Growth and Enhances Radiosensitivity in Oral Squamous Cell Carcinoma by Targeting Insulin Like Growth Factor 1 Receptor

Colorectal cancer (CRC) is one of the most common malignancies in the world. Easier recurrence and metastasis is the main cause of mortality in CRC patients, and the markers applied for diagnosis and treatment of CRC is still urgently needed to early diagnose and evaluate therapeutic effect. Long noncoding RNA (lncRNA) is a class of noncoding RNA that the length is more than 200 nucleotides. With the development of sequencing technique about transcriptome, increasing lncRNAs are focused on their function and mechanism related to the nosogenesis and pathology of CRC. Recent studies report that lncRNAs acted as crucial role in CRC and could be as biomarker for CRC diagnosis and treatment. In this review, we display the regulation of lncRNA by interacting with DNA, RNA and protein and highlight the double role of lncRNAs as oncogene or anti-tumor gene involved in Wnt signaling pathway, p53 signaling pathway or others to be an regulator in CRC development. Lastly, we discuss some new finding of lncRNAs, especially lncRNA in exosome, which could be as potential markers for diagnosis and treatment of CRC in future.

Zhenqiang Sun

Jinbo Liu

Chen Chen

Quanbo Zhou

Shuaixi Yang

Guixian Wang

Junmin Song

Zhen Li

Zhiyong Zhang

Jizhong Xu

Xiantao Sun

Yuan Chang

Weitang Yuan

The Biological Effect and Clinical Application of Long Noncoding RNAs in Colorectal Cancer

Tendons play a crucial role in the musculoskeletal system, connecting muscles to bones and enabling efficient force transfer. However, they are prone to acute and chronic injuries, which, if not properly repaired, can significantly impair function. Tendinopathy, a prevalent condition affecting approximately 20% of musculoskeletal complaints, arises from an imbalance between micro-injury accumulation and repair processes. The extracellular matrix (ECM) of tendons is a hierarchical structure comprising collagen fibrils, proteoglycans, and glycoproteins that regulate organization, hydration, and mechanical properties. Mechanotransduction pathways, mediated by integrins and focal adhesion complexes, activate signaling cascades such as MAPK/ERK and PI3K/Akt, driving tenocyte gene expression and ECM remodeling. Adaptations to load involve region-specific remodeling, with tensile regions favoring aligned Type I collagen and compressive regions promoting proteoglycans like aggrecan. Stress shielding or reduced loading disrupts these pathways, leading to matrix disorganization and inflammation, predisposing tendons to degenerative changes. Insights into these molecular mechanisms inform rehabilitation strategies to enhance tendon repair and mitigate tendinopathy progression in both athletic and general populations.

Mikołaj Stańczak

Bartłomiej Kacprzak

Piotr Gawda

Tendon Cell Biology: Effect of Mechanical Loading

肌腱细胞生物学：机械负荷的影响

The nano-method has been used as a technique for creating novel, non-traditional antimicrobial agents. This effective method for treating infectious diseases has many advantages over conventional antibiotics, including increased efficacy against species that have developed drug resistance, and the ability to circumvent the development of resistance that disrupts a number of biological pathways. As a result, the objective of this study was to synthesize and characterize silver nanoparticles using phenolic compounds obtained from

Hawazen Salih

Rami Altameemi

Ahmed Al-Azawi

Antibacterial Activity of Silver Nanoparticles Prepared from Camellia Sinensis Extracts in Multi-Drug Resistant Staphylococcus Aureus

茶树提取物制备的银纳米粒子对耐多药金黄色葡萄球菌的抗菌活性

Background/Aims: Lead exposure is known to induce oxidative stress and neurotoxicity. Nitric oxide (NO) plays an important role in modulating oxidative stress, with L-arginine as a precursor of NO and Nω-nitro-L-arginine (L-NNA) as an inhibitor of NO synthase, an enzyme that catalyses the production of nitric oxide (NO) from L-arginine. Methods: This study investigated the differential effects of L-arginine and L-NNA on markers of oxidative stress and biochemical changes in brain tissue from rats with different levels of resistance to hypoxia exposed to lead nitrate. Rats with either low or high resistance to hypoxia were exposed to lead nitrate (oral 3.6 mg lead nitrate/kg b.w. per day for 30 days) and treated with L-arginine (600 mg/kg b.w., i.p., 30 min before and after exposure to lead nitrate) or L-NNA (35 mg/kg b.w., i.p., 30 min before and after exposure to lead nitrate). Brain tissue samples were analysed for lipid peroxidation, oxidative modification of proteins, and activity of antioxidant enzymes, including superoxide dismutase, catalase, glutathione reductase, and peroxidase, and total antioxidant status (TAS). We also examined the biomarkers of biochemical pathways involving the activity of alanine and aspartate aminotransferases, succinate dehydrogenase (SDH), and α-ketoglutarate dehydrogenase (KGDH). In addition, the trend observed was supported by assessments of the acetylcholine levels and acetylcholinesterase activity (ACh-AChE system) in brain tissue. Results: In rats with low resistance to hypoxia, the L-arginine treatment significantly reduced lipid peroxidation and oxidative protein modification but increased antioxidant enzyme activity, suggesting a protective effect against lead-induced oxidative stress. Conversely, in rats with high resistance to hypoxia, L-NNA had a protective effect, reducing lead-induced oxidative damage and decreasing lipid peroxidation, whereas L-arginine exacerbated oxidative stress and impaired antioxidant defences. These findings were supported by corresponding changes in the acetylcholine-acetylcholinesterase system, reflecting the observed patterns of lead-induced oxidative stress and neurotoxicity. The study shows that L-arginine exerts a protective effect by reducing lead-induced oxidative damage via an improvement in TAS. Our study shows that lead nitrate exposure significantly increases ala-nine and aspartate aminotransferase activity in brain tissue, with L-arginine exacerbating and L-NNA reversing this effect. The lead nitrate exposure also affected the activities of SDH and KGDH, which are important for cellular energy production and hypoxia resistance, with L-arginine altering SDH activity depending on the level of resistance and L-NNA enhancing both SDH and KGDH activities. These trends were further validated by alterations in the ACh-AChE system, highlighting the differential role of NO-dependent mechanisms in modulating lead-induced neurotoxicity based on hypoxia resistance. Conclusion: These findings suggest potential targeted therapeutic strategies based on the oxidative stress profile and highlight the potential of nitric oxide system modulators in counteracting lead-induced biochemical alterations and the dynamics of the ACh-AChE system depending on the individual physiological reactivity of organisms.

Natalia Kurhaluk

Piotr Kamiński

Oleksandr Lukash

Halina Tkaczenko

Nitric Oxide-Dependent Regulation of Oxygen-Related Processes in a Rat Model of Lead Neurotoxicity: Influence of the Hypoxia Resistance Factor

一氧化氮依赖性调节氧相关过程在大鼠铅神经毒性模型中的作用：缺氧抵抗因子的影响

Breast cancer is the most frequent cancer among women. Despite extensive research in recent years the molecular basis of breast cancer development, growth and metastasis remains unclear. Numerous studies highlight the involvement of BMI-1 in tumorigenesis. BMI-1 protein is a key component of Polycomb Repressive Complex 1, which by ubiquitinylation of histone H2A, regulates expression of genes involved in various cellular processes including cell cycle, proliferation and programmed cell death. Overexpression of BMI-1 has been often associated with breast cancer development and progression. This review summarizes the current state of knowledge of BMI-1's role in breast cancer biology and its potential significance as prognostic marker and potential target of new anticancer therapy.

Aleksandra Szustka

Anna Krześlak

BMI-1 in Breast Cancer – Biological Role and Clinical Implications

BMI-1在乳腺癌中的生物学作用及临床意义

Background/Aims: Atherosclerotic cardiovascular disease (ASCVD) or atherosclerosis is a chronic condition that is incurable and a leading contributor to morbidity and mortality. However, it is easy to prevent ASCVD by managing or preventing risk factors like hyperlipidemia, obesity/overweight, hypertension, and diabetes. This systematic review summarizes and presents current evidence on whether physical exercise could help in reducing ASCVD risk factors. Materials: A comprehensive search was performed on PubMed, CINAHAL, ProQuest and Google Scholar. The sources were assessed based on their peer-review status, description of methods, unavailability of full texts, publication date (less than seven years), and publication in the English Language. The final search results constituted 19 peer-reviewed articles. Results: Physical exercise is effective in improving the lipid profile, reducing waist circumference, reducing blood pressure, and lowering blood glucose levels. All types of physical exercise with intensity varying from low to high yield positive outcomes, although there is no consensus on whether the physical exercise program should be implemented for three months or less or on a long-term basis. Conclusion: Physical exercise prevents and improves the management of hyperlipidemia, obesity/overweight, hypertension, and diabetes, which makes it a good intervention for reducing the risk of ASCVD. However, further studies should be performed to determine the duration within which the intervention should be sustained for optimal results.

Nada Alhazmi

The Effectiveness of Physical Exercise in Reducing Common Risk Factors of Atherosclerosis: A Systematic Review

体力活动在降低动脉粥样硬化常见风险因素中的有效性：一项系统综述

Abbreviation	Cell Physiol Biochem
Journal Impact	2.44
Quartiles(Global)	PHYSIOLOGY(Q2)

ISSN	1015-8987, 1421-9778
h-index	112

Publication Information	Publisher: Cell Physiol Biochem Press GmbH & Co KG，Publishing cycle: Bimonthly，Journal Type: journal，Open Access Journals: Yes
Basic data	Year of publication: 1991，Proportion of original research papers: 0.00%，Self Citation Rate:4.00%， Gold OA Rate: 98.73%
Journal Fees	$Details
Average review cycle	网友分享经验：平均1月
Average recruitment ratio	网友分享经验：约95%

Cellular Physiology and Biochemistry

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