BIOGERONTOLOGY 杂志提供了一个研究平台，主要旨在实现健康的晚年并延长寿命。重点是努力理解、预防、治愈或尽量减少与年龄相关的损伤。BIOGERONTOLOGY 提供了一个同行评审论坛，用于发布关于通过物理、化学和生物手段（包括转基因）调节衰老过程的原始研究数据、新想法和讨论和淘汰生物；细胞培养系统，以开发新方法和保健产品，以维持或恢复失去的生化功能；免疫学、自身免疫和衰老中的感染；脊椎动物、无脊椎动物、微生物和植物，用于老化和长寿的遗传决定因素的实验研究；将衰老和生存动力学联系起来的生物人口学和理论模型。

The journal Biogerontology provides a research platform aimed at promoting healthy aging and extending lifespan. It focuses on understanding, preventing, treating, or minimizing age-related damage. Biogerontology offers a peer-reviewed forum for publishing original research data, new ideas, and discussions on the modulation of the aging process through physical, chemical, and biological means, including genetic engineering. Topics include the development of cell culture systems to create new methods and health products to maintain or restore lost biochemical functions; immunology, autoimmunity, and infections in aging; experimental studies on genetic determinants of aging and longevity in vertebrates, invertebrates, microorganisms, and plants; and biostatistical and theoretical models linking aging with survival dynamics.

BIOGERONTOLOGY杂志提供了一个研究平台，旨在促进健康的晚年并延长寿命。该期刊重点关注理解、预防、治疗或尽量减少与年龄相关的损伤。BIOGERONTOLOGY为同行评审提供了一个论坛，发布关于通过物理、化学和生物手段（包括转基因技术）调节衰老过程的原创研究数据、新思想及讨论。内容涵盖细胞培养系统的开发，以创造新方法和保健产品，维持或恢复失去的生化功能；免疫学、自身免疫及衰老中的感染；脊椎动物、无脊椎动物、微生物和植物的实验研究，探讨老化和长寿的遗传决定因素；以及将衰老与生存动力学联系起来的生物人口学和理论模型。

Biogerontology

Our previous findings indicate that the gastrocnemius muscle of aging rats exhibits impairments of muscle quality (force/unit muscle tissue) and autophagy and increased sarcoplasmic reticulum stress. The purpose of this study was to examine age-related changes in soleus muscle contractility and in markers of autophagy in the soleus and gastrocnemius muscles. We assessed in situ muscle force and size in the soleus muscle of adult (7-8 months) and aged (24-26 months) male, F344/BN rats. We used immunoblotting to compare abundance of markers of autophagy, sarcoplasmic reticulum (SR) stress and sphingolipid metabolism in the soleus and medial gastrocnemius (MG) muscles of these animals. Relative to adults, aged rats maintained soleus muscle quality and increased muscle size, resulting in increased tetanic force production. Immunoblotting revealed a general pattern of an age-related reduction of basal autophagy, despite increases in indicators of SR stress and upstream autophagic pathway activation in the MG. The MG also exhibited changes in markers of sphingolipid metabolism suggestive of increased muscle ceramide. Minimal age-related changes were observed in the soleus. The soleus maintains muscle mass and quality with age, and exhibits fewer age-related changes in markers of stress and autophagy than the MG. Based on these data, we suggest that maintenance of autophagy may preserve muscle quality by preventing excessive SR stress.

David W Russ

Iva M Boyd

Katherine M McCoy

Katherine W McCorkle

Muscle-specificity of age-related changes in markers of autophagy and sphingolipid metabolism.

年龄相关变化在自噬和鞘脂代谢标志物中的肌肉特异性。

Ageing is an inevitable and multifaceted biological process that impacts a wide range of cellular and molecular mechanisms, leading to the development of various diseases, such as liver fibrosis. Liver fibrosis progresses to cirrhosis, which is an advanced form due to high amounts of extracellular matrix and restoration of normal liver structure with failure to repair damaged tissue and cells, marking the end of liver function and total liver failure, ultimately death. The most important factors are reactive oxygen species (ROS) and cellular senescence. Oxidative stress is defined as an impairment by ROS, which are by-products of the mitochondrial electron transport chain and other key molecular pathways that induce cell damage and can activate cellular senescence pathways. Cellular senescence is characterized by pro-inflammatory cytokines, growth factors, and proteases secreted by senescent cells, collectively known as the senescence-associated secretory phenotype (SASP). The presence of senescent cells, which disrupt tissue architecture and function and increase senescent cell production in liver tissues, contributes to fibrogenesis. Hepatic stellate cells (HSCs) are activated in response to chronic liver injury, oxidative stress, and senescence signals that drive excessive production and deposition of extracellular matrix. This review article aims to provide a comprehensive overview of the pathogenic role of ROS and cellular senescence in the aging liver and their contribution to fibrosis.

Waleed Hassan Almalki

Salem Salman Almujri

Aging, ROS, and cellular senescence: a trilogy in the progression of liver fibrosis

衰老、活性氧和细胞衰老：肝纤维化进展的三部曲

To facilitate the process of aging healthily and prevent age-related health problems, efforts to properly understand aging mechanisms and develop effective and affordable anti-aging interventions are deemed necessary. Systemic administration of D-galactose has been established to artificially induce senescence in vitro and in vivo as well as for anti-aging therapeutic interventions studies. The aim of this article is to comprehensively discuss the use of D-galactose to generate a model of accelerated aging and its possible underlying mechanisms involved in different tissues/organs.

Khairunnuur Fairuz Azman

Rahimah Zakaria

D-Galactose-induced accelerated aging model: an overview.

D-半乳糖诱导的加速衰老模型：综述。

Malnutrition due to aging is partly caused by decreased absorption of nutrients by the gastrointestinal tract. However, the underlying mechanism is unclear and changes in lipid absorption with aging are poorly understood. In this study, changes in lipid absorption with aging were examined in mice aged 3 and 25 months. After overnight fasting, blood samples were collected from snipped tails and then soybean oil was administered orally. Three hours later, mice were sacrificed by decapitation and the liver, pancreas, small intestine and blood were collected. The increase in serum triacylglycerol after soybean oil administration was significantly lower in the older mice, indicating a decrease in lipid absorption with aging. Measurement of mRNA levels for triacylglycerol absorption-related genes showed that mRNA for pancreatic lipase tended to decrease in 25-month-old mice. There was no significant difference in the protein level of pancreatic lipase, but the enzyme activity showed a significant decrease in the older mice. To examine this mechanism, expression levels of mRNA for protein turnover-related genes in the pancreas were measured. The level of a proteasomal mRNA showed a significant decrease in 25-month-old mice. This suggests that the ability to degrade unfolded protein decreases in the aging pancreas, and that this leads to reduction of pancreatic lipase activity and a decrease in lipid absorption.

Kazushi Yamamoto

Yasuna Kitano

E Shuang

Yu Hatakeyama

Yu Sakamoto

Taro Honma

Tsuyoshi Tsuduki

Decreased lipid absorption due to reduced pancreatic lipase activity in aging male mice.

衰老雄性小鼠胰脂肪酶活性降低导致脂质吸收减少。

Blood cells are crucial components of the human body, closely linked to the aging process. This study aims to explore the causal relationship between 91 blood cell phenotypes and aging through Mendelian randomization (MR) analysis. Exposure data from genome-wide association studies (GWAS) was extracted from the GWAS of blood cell perturbation phenotypes in 2,600 European individuals. Initial analysis utilized GWAS data related to aging from the GWAS Catalog database GCST90014288, with inverse-variance weighting as the primary method for causal analysis. Sensitivity analyses included Cochran's Q test, MR-Egger intercept test, MR-PRESSO, and leave-one-out analysis. For significant associations, replication and meta-analysis were conducted using independent aging GWAS data from GCST90014300. Initial analysis revealed that environmental peroxide-impacted red blood cells and ciprofloxacin-impacted reticulocytes accelerated aging. Additionally, elevated neutrophil levels were found to accelerate aging, while LiCl-impacted neutrophils reduced aging risk. Replication and meta-analysis showed consistent results: ciprofloxacin-impacted reticulocytes and elevated neutrophil levels increased the risk of aging, while LiCl-impacted neutrophils reduced the risk. RBCs showed no significant impact on aging progression. Sensitivity analyses confirmed the robustness and reliability of these positive findings. Our study provides evidence of a causal relationship between three blood cell disturbance phenotypes and human aging.

Jingjing Zhang

Xin Zhang

Boan Xiao

Jiecai Ouyang

Peng Wang

Xiaobin Peng

Analyzing the causal role of blood cells in aging: a Mendelian randomization study

分析血液细胞在衰老中的因果作用：一项孟德尔随机化研究

Cardiomyocyte senescence plays a crucial role in the pathophysiology of age-related cardiovascular disease. Senescent cells with impaired contractility, mitochondrial dysfunction, and hypertrophic growth accumulate in the heart during aging, contributing to cardiac dysfunction and remodeling. Mitochondrial dynamics is altered in aging cells, leading to changes in their function and morphology. Such rearrangements can affect the spatially restricted region of the mitochondrial membrane that interacts with reticulum membrane fragments, termed mitochondria-endoplasmic reticulum (ER) contact sites (MERCs). Besides, oxidative stress associated with inefficient organelle turnover can drive cellular senescence. Therefore, in this study, we evaluated the possible association between the senolytic effect of the antioxidant quercetin (Q) and MERCs preservation in a D-galactose-induced cellular senescence model. We found that Q ameliorates the senescent phenotype of H9c2 cells in association with increased mitochondria-ER colocalization, reduced distance between both organelles, and lower ROS production. Moreover, regulation of fusion and fission processes was related with increased mitochondrial ATP production and enhanced transmembrane potential. Overall, our data provide evidence that the inhibitory effect of Q on cellular senescence is associated with preserved MERCs and improved mitochondrial function and morphology, which might contribute to the attenuation of cardiac dysfunction.

Ray Jiménez

Alejandra Zúñiga-Muñoz

Edith Álvarez-León

Wylly Ramsés García-Niño

Gabriela Navarrete-Anastasio

Elizabeth Soria-Castro

Israel Pérez-Torres

Elizabeth Lira-Silva

Natalia Pavón

Alfredo Cruz-Gregorio

Rebeca López-Marure

Cecilia Zazueta

Alejandro Silva-Palacios

Quercetin preserves mitochondria-endoplasmic reticulum contact sites improving mitochondrial dynamics in aged myocardial cells

槲皮素通过保护线粒体-内质网接触点改善衰老心肌细胞的线粒体动力学

The aging population faces a gradual decline in physical and mental capacities, with an increased risk of liver cirrhosis and chronic liver diseases leading to hepatic encephalopathy (HE). The intertwining of physiological manifestations of aging with the pathophysiology of HE significantly impairs cognitive ability, reduces quality of life, and increases mortality. Hence, effective therapeutic intervention is imperative. The present study investigated the impact of minimal HE (MHE) on cognitive impairment in an aged rat population by analyzing hippocampal proteome dynamics. For this purpose, an old MHE rat model was induced via thioacetamide. The label-free LC‒MS/MS method was employed to explore hippocampal proteomic changes and associated dysregulated biological pathways. A total of 1533 proteins were identified, and among these, 30 proteins were significantly differentially expressed (18 upregulated, and 12 downregulated). Three upregulated proteins, namely, fetuin-A, p23, and intersectin-1 were selected and validated for their increased expression via western blotting and immunofluorescence analysis, which confirmed the mass spectrometry results. These proteins have not been reported previously in MHE cases. We also identified the possible dysregulated biological pathways associated with the differentially expressed proteins via Metascape, a network analysis tool. We found that the differentially expressed proteins may be involved in the generation of precursor metabolites and energy, the neurotransmitter release cycle, positive regulation of dendritic spine development, chaperone-mediated protein folding and protein stabilization. This study highlights the potential mechanisms underlying neurological dysfunction in the aged population with MHE and identifies novel therapeutic targets for improved disease management.

Vishal Vikram Singh

Shambhu Kumar Prasad

Arup Acharjee

Sanjeeva Srivastava

Papia Acharjee

Investigating cognitive impairments and hippocampal proteome alterations in aged male rats with TAA-Induced minimal hepatic encephalopathy

研究硫代乙酰胺诱导的轻微肝性脑病老年雄性大鼠的认知障碍和海马蛋白质组变化

Advanced Glycation End (AGE) products are one such factor that accumulates during aging and age-related diseases. However, how exogenous AGE compounds cause aging is an area that needs to be explored. Specifically, how an organ undergoes aging and aging-related phenomena that need further investigation. The intestine is the most exposed area to food substances. How AGEs affect the intestine in terms of aging need to be explored. Drosophila melanogaster, a well-known model organism, is used to decode aging and age-associated phenomena. In this study, we fed Ribose induced Advanced Glycation End products (Rib-AGE) to D. melanogaster to study the aging mechanism. The Rib-AGE-induced aging was checked in Drosophila. We found a series of changes in Rib-AGE-fed flies. Reactive oxygen species (ROS) and nitric oxide species (NOs) were higher in the Rib-AGE-fed flies, and the antioxidant level was lower. The intestinal permeability was altered. The microorganism load was higher inside the gut. The structural arrangement of the gut's microfilament was found to be damaged, and the nuclear shape was found to be irregular. Cell death within the gut was elevated in comparison to control. The food intake was found to be reduced. The relative mRNA expression of the Sirtuin 2 and Sirtuin 6 gene of D. melanogaster was downregulated in Rib-AGE-fed flies compared to the control. All these findings strongly suggest that Rib-AGE accelerates aging and age-related disorders in D. melanogaster.

Lokanath Mishra

Monalisa Mishra

Ribose-induced advanced glycation end products reduce the lifespan in Drosophila melanogaster by changing the redox state and down-regulating the Sirtuin genes

核糖诱导的晚期糖基化终产物通过改变氧化还原状态和下调Sirtuin基因缩短黑腹果蝇的寿命

Uncouplers of mitochondrial electron transport chain, such as 2,4-dinitrophehol (DNP), can mimic calorie restriction by decreasing efficiency of adenosine triphosphate (ATP) synthesis. However, DNP is also a toxic substance, whose overdosage can be lethal. In the fruit fly, Drosophila melanogaster model, we have found that DNP in concentrations of 0.05-0.2 g/L, led to a drastic decrease in fruit fly survival on a low caloric diet (1% sucrose and 1% yeast; 1S-1Y). On the 5S-5Y diet, DNP decreased lifespan of flies reared only in concentration 0.2 g/L, whilst on the diet 15S-15Y DNP either did not significantly shortened fruit fly lifespan or extended it. The lifespan extension on the high caloric 15S-15Y diet with DNP was accompanied by lower activity of lactate dehydrogenase and a decrease in activities of mitochondrial respiratory chain complexes I, II, and V, determined by blue native electrophoresis followed by in-gel activity assays. The exposure to DNP also did not affect key glycolytic enzymes, antioxidant and related enzymes, and markers of oxidative stress, such as aconitase activity and amount protein carbonyls. Consumption of DNP-supplemented diet did not affect flies' resistance to heat stress, though made male flies slightly more resistant to starvation compared with males reared on the control food. We also did not observe substantial changes in the contents of metabolic stores, triacylglycerols and glycogen, in the DNP-treated flies. All this suggest that a nutrient-rich diets provide effective protection against DNP, providing a mild uncoupling of the respiratory chain that allows lifespan extension without considerable changes in metabolism.

Olha M. Strilbytska

Uliana Semaniuk

Ihor Yurkevych

Vladyslav Berezovskyi

Andriy Glovyak

Dmytro V. Gospodaryov

Maria M. Bayliak

Oleh Lushchak

2,4-Dinitrophenol is toxic on a low caloric diet but extends lifespan of Drosophila melanogaster on nutrient-rich diets without an impact on metabolism

2,4-二硝基苯酚在低热量饮食下具有毒性，但在营养丰富的饮食中延长了果蝇的寿命且不影响代谢

Zsolt Radak

Suresh I. S. Rattan

Exercise, hormesis and ageing: a new section in Biogerontology

运动、毒物兴奋效应与衰老：生物老年学新专栏

Abbreviation
Journal Impact	4.39
Quartiles(Global)	GERIATRICS & GERONTOLOGY(Q1)

ISSN	1389-5729, 1573-6768
h-index	91

Publication Information	Publisher: Springer Science and Business Media B.V.，Publishing cycle: Quarterly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 2000，Proportion of original research papers: 77.78%，Self Citation Rate:6.80%， Gold OA Rate: 18.63%
Average review cycle	网友分享经验：>12周，或约稿
Average recruitment ratio	网友分享经验：一般

Biogerontology

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