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The potential use of nanozyme in aging and age‐related diseases 纳米酶在衰老和老年相关疾病中的潜在用途
IF 4.5 4区 医学 Q1 Nursing Pub Date : 2024-03-11 DOI: 10.1007/s10522-024-10095-w
Amirsasan Gorgzadeh, Paria Arab Amiri, Saman Yasamineh, Basim Kareem Naser, Khairia abdulrahman abdulallah

The effects of an increasingly elderly population are among the most far-reaching in 21st-century society. The growing healthcare expense is mainly attributable to the increased incidence of chronic illnesses that accompany longer life expectancies. Different ideas have been put up to explain aging, but it is widely accepted that oxidative damage to proteins, lipids, and nucleic acids contributes to the aging process. Increases in life expectancy in all contemporary industrialized cultures are accompanied by sharp increases in the prevalence of age-related diseases such as cardiovascular and neurological conditions, type 2 diabetes, osteoporosis, and cancer. Therefore, academic and public health authorities should prioritize the development of therapies to increase health span. Nanozyme (NZ)-like activity in nanomaterials has been identified as promising anti-aging nanomedicines. More than that, nanomaterials displaying catalytic activities have evolved as artificial enzymes with high structural stability, variable catalytic activity, and functional diversity for use in a wide range of biological settings, including those dealing with age-related disorders. Due to their inherent enzyme-mimicking qualities, enzymes have attracted significant interest in treating diseases associated with reactive oxygen species (ROS). The effects of NZs on aging and age-related disorders are summarized in this article. Finally, prospects and threats to enzyme research and use in aging and age-related disorders are offered.

Graphical Abstract

老年人口日益增多对 21 世纪社会的影响最为深远。医疗费用不断增长的主要原因是,随着预期寿命的延长,慢性病的发病率也在增加。人们提出了不同的观点来解释衰老,但普遍认为蛋白质、脂类和核酸的氧化损伤是衰老过程的原因。在所有当代工业化文化中,预期寿命延长的同时,与年龄有关的疾病,如心血管和神经系统疾病、2 型糖尿病、骨质疏松症和癌症的发病率也急剧上升。因此,学术界和公共卫生部门应优先开发延长健康寿命的疗法。纳米材料中的纳米酶(NZ)类活性已被确认为有前途的抗衰老纳米药物。不仅如此,具有催化活性的纳米材料已发展成为具有高结构稳定性、可变催化活性和功能多样性的人工酶,可用于各种生物环境,包括与年龄有关的疾病。由于具有模仿酶的固有特性,酶在治疗与活性氧(ROS)有关的疾病方面引起了极大的兴趣。本文概述了 NZs 对衰老和老年相关疾病的影响。最后,提出了在衰老和与年龄有关的疾病中研究和使用酶的前景和威胁。
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引用次数: 0
The SGLT2 inhibitor empagliflozin inhibits skeletal muscle fibrosis in naturally aging male mice through the AMPKα/MMP9/TGF-β1/Smad pathway SGLT2抑制剂empagliflozin通过AMPKα/MMP9/TGF-β1/Smad途径抑制自然衰老雄性小鼠的骨骼肌纤维化
IF 4.5 4区 医学 Q1 Nursing Pub Date : 2024-02-26 DOI: 10.1007/s10522-024-10093-y

Abstact

With advancing age, the incidence of sarcopenia increases, eventually leading to a cascade of adverse events. However, there is currently a lack of effective pharmacological treatment for sarcopenia. Sodium-glucose co-transporter 2 inhibitor (SGLT2i) empagliflozin demonstrates anti-fibrotic capabilities in various organs. This study aims to determine whether empagliflozin can improve skeletal muscle fibrosis induced by sarcopenia in naturally aging mice. A natural aging model was established by feeding male mice from 13 months of age to 19 months of age. A fibrosis model was created by stimulating skeletal muscle fibroblasts with TGF-β1. The Forelimb grip strength test assessed skeletal muscle function, and expression levels of COL1A1, COL3A1, and α-SMA were analyzed by western blot, qPCR, and immunohistochemistry. Additionally, levels of AMPKα/MMP9/TGFβ1/Smad signaling pathways were examined. In naturally aging mice, skeletal muscle function declines, expression of muscle fibrosis markers increases, AMPKα expression is downregulated, and MMP9/TGFβ1/Smad signaling pathways are upregulated. However, treatment with empagliflozin reverses this phenomenon. At the cellular level, empagliflozin exhibits similar anti-fibrotic effects, and these effects are attenuated by Compound C and siAMPKα. Empagliflozin exhibits anti-fibrotic effects, possibly associated with the AMPK/MMP9/TGFβ1/Smad signaling pathways.

停用 随着年龄的增长,肌肉疏松症的发病率也会增加,最终导致一系列不良反应。然而,目前还缺乏治疗肌肉疏松症的有效药物。钠-葡萄糖协同转运体 2 抑制剂(SGLT2i)empagliflozin 在多个器官中显示出抗纤维化能力。本研究旨在确定empagliflozin能否改善自然衰老小鼠因肌肉疏松症诱发的骨骼肌纤维化。通过喂养 13 个月至 19 个月大的雄性小鼠,建立了自然衰老模型。通过用 TGF-β1 刺激骨骼肌成纤维细胞建立了纤维化模型。前肢握力测试评估了骨骼肌功能,并通过Western印迹、qPCR和免疫组化分析了COL1A1、COL3A1和α-SMA的表达水平。此外,还检测了 AMPKα/MMP9/TGFβ1/Smad 信号通路的水平。在自然衰老的小鼠中,骨骼肌功能下降,肌肉纤维化标志物表达增加,AMPKα表达下调,MMP9/TGFβ1/Smad信号通路上调。然而,使用empagliflozin治疗可逆转这一现象。在细胞水平,empagliflozin表现出类似的抗纤维化作用,而化合物C和siAMPKα会减弱这些作用。Empagliflozin 的抗纤维化作用可能与 AMPK/MMP9/TGFβ1/Smad 信号通路有关。
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引用次数: 0
A CRISPR base editing approach for the functional assessment of telomere biology disorder-related genes in human health and aging 用 CRISPR 碱基编辑方法对人类健康和衰老过程中端粒生物学紊乱相关基因进行功能评估
IF 4.5 4区 医学 Q1 Nursing Pub Date : 2024-02-04 DOI: 10.1007/s10522-024-10094-x
Gustavo Borges, Yahya Benslimane, Lea Harrington

Telomere Biology Disorders (TBDs) are a group of rare diseases characterized by the presence of short and/or dysfunctional telomeres. They comprise a group of bone marrow failure syndromes, idiopathic pulmonary fibrosis, and liver disease, among other diseases. Genetic alterations (variants) in the genes responsible for telomere homeostasis have been linked to TBDs. Despite the number of variants already identified as pathogenic, an even more significant number must be better understood. The study of TBDs is challenging since identifying these variants is difficult due to their rareness, it is hard to predict their impact on the disease onset, and there are not enough samples to study. Most of our knowledge about pathogenic variants comes from assessing telomerase activity from patients and their relatives affected by a TBD. However, we still lack a cell-based model to identify new variants and to study the long-term impact of such variants on the genes involved in TBDs. Herein, we present a cell-based model using CRISPR base editing to mutagenize the endogenous alleles of 21 genes involved in telomere biology. We identified key residues in the genes encoding 17 different proteins impacting cell growth. We provide functional evidence for variants of uncertain significance in patients with TBDs. We also identified variants resistant to telomerase inhibition that, similar to cells expressing wild-type telomerase, exhibited increased tumorigenic potential using an in vitro tumour growth assay. We believe that such cell-based approaches will significantly advance our understanding of the biology of TBDs and may contribute to the development of new therapies for this group of diseases.

端粒生物学疾病(TBDs)是一组以端粒过短和/或端粒功能障碍为特征的罕见疾病。它们包括一组骨髓衰竭综合征、特发性肺纤维化和肝病等疾病。负责端粒平衡的基因中的遗传变异(变体)与TBDs有关。尽管有许多变体已被确定为致病基因,但仍有更多的变体需要更好地了解。对 TBDs 的研究具有挑战性,因为这些变异因其罕见性而难以确定,很难预测它们对疾病发病的影响,而且也没有足够的样本可供研究。我们对致病变异的了解大多来自于对TBD患者及其亲属端粒酶活性的评估。然而,我们仍然缺乏一个基于细胞的模型来识别新的变异体,并研究这些变异体对TBDs相关基因的长期影响。在这里,我们提出了一种基于细胞的模型,利用 CRISPR 碱基编辑技术诱变参与端粒生物学的 21 个基因的内源等位基因。我们确定了编码 17 种不同蛋白质的基因中影响细胞生长的关键残基。我们为 TBDs 患者中意义不明的变异提供了功能性证据。我们还发现了对端粒酶抑制具有抗性的变体,这些变体与表达野生型端粒酶的细胞类似,在体外肿瘤生长试验中表现出更高的致瘤潜力。我们相信,这种基于细胞的方法将极大地推动我们对TBDs生物学的了解,并可能有助于开发治疗这类疾病的新疗法。
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引用次数: 0
Fisetin, a potential skin rejuvenation drug that eliminates senescent cells in the dermis. Fisetin,一种潜在的皮肤再生药物,可以消除真皮中的衰老细胞。
IF 4.5 4区 医学 Q1 Nursing Pub Date : 2024-02-01 Epub Date: 2023-09-22 DOI: 10.1007/s10522-023-10064-9
Kento Takaya, Toru Asou, Kazuo Kishi

Accumulation of senescent fibroblasts, chronic inflammation, and collagen remodeling due to aging-related secretory phenotypes have been hypothesized to cause age-related skin aging, which results in wrinkles and loss of skin elasticity, thus compromising appearance attractiveness. However, the rejuvenating effects of removing senescent cells from the human skin and the efficacy of related therapeutic agents remain unclear. Here, we investigated the effects of fisetin, a potential anti-aging component found in various edible fruits and vegetables, on senescent human dermal fibroblasts (HDFs) and aging human skin. Senescence was induced in primary HDFs using long-term passaging and treatment with ionizing radiation, and cell viability was assessed after treatment with fisetin and a control component. A mouse/human chimeric model was established by subcutaneously transplanting whole skin grafts from aged individuals into nude mice, which were treated intraperitoneally with fisetin or control a component for 30 d. Skin samples were obtained and subjected to senescence-associated-beta-galactosidase staining; the extent of aging was evaluated using western blotting, reverse transcription-quantitative PCR, and histological analysis. Fisetin selectively eliminated senescent dermal fibroblasts in both senescence-induced cellular models; this effect is attributable to cell death induction by caspases 3, 8, and 9-mediated endogenous and exogenous apoptosis. Fisetin-treated senescent human skin grafts showed increased collagen density and decreased senescence-associated secretory phenotypes (SASP), including matrix metalloproteinases and interleukins. No apparent adverse events were observed. Thus, fisetin could improve skin aging through selective removal of senescent dermal fibroblasts and SASP inhibition, indicating its potential as an effective novel therapeutic agent for combating skin aging.

衰老成纤维细胞的积累、慢性炎症和衰老相关分泌表型引起的胶原重塑被认为会导致与年龄相关的皮肤衰老,从而导致皱纹和皮肤弹性丧失,从而损害外观吸引力。然而,从人类皮肤中去除衰老细胞的再生作用和相关治疗剂的疗效尚不清楚。在这里,我们研究了在各种可食用水果和蔬菜中发现的一种潜在的抗衰老成分非西汀对衰老的人类真皮成纤维细胞(HDFs)和衰老的人类皮肤的影响。使用长期传代和电离辐射处理在原发性HDFs中诱导衰老,并在用非西汀和对照组分处理后评估细胞活力。通过将来自老年人的整个皮肤移植物皮下移植到裸鼠中来建立小鼠/人嵌合模型,裸鼠用非西汀或对照A组分腹膜内处理30d。获得皮肤样品并进行衰老相关的β-半乳糖苷酶染色;使用蛋白质印迹、逆转录定量PCR和组织学分析来评估衰老程度。在两种衰老诱导的细胞模型中,Fisetin选择性地消除衰老的真皮成纤维细胞;这种作用可归因于胱天蛋白酶3、8和9介导的内源性和外源性细胞凋亡诱导的细胞死亡。Fisetin处理的衰老人类皮肤移植物显示出胶原密度增加和衰老相关分泌表型(SASP)降低,包括基质金属蛋白酶和白细胞介素。未观察到明显的不良事件。因此,非西汀可以通过选择性去除衰老的真皮成纤维细胞和抑制SASP来改善皮肤衰老,这表明它有潜力成为一种有效的新型治疗剂来对抗皮肤衰老。
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引用次数: 0
Heat-induced hormesis in longevity is linked to heat-stress sensitivity across laboratory populations from diverse altitude of origin in Drosophila buzzatii. 热诱导的长寿兴奋症与来自不同海拔高度的果蝇实验室种群的热应激敏感性有关。
IF 4.5 4区 医学 Q1 Nursing Pub Date : 2024-02-01 Epub Date: 2023-09-19 DOI: 10.1007/s10522-023-10066-7
Mariano Almirón, Federico H Gomez, Pablo Sambucetti, Fabian M Norry

Heat-induced hormesis in longevity is the increase in life span resulting from the previous exposure to a mild heat stress early in life. Here we examined heat-induced hormesis of Drosophila buzzatii in five mass-mating populations, which were derived from five wild populations along an elevation gradient from 202 to 1855 m above sea level in North-Western Argentina. Five day old flies were exposed to 37.5 °C for 90 min to induce hormesis and its possible variation across altitudinal populations. This heat treatment strongly extended longevity in lowland-derived flies from the most heat-resistant population only. Both heat-induced effects on longevity and heat-knockdown time (heat-stress sensitivity) were negatively correlated to altitude of population of origin. Hormesis was positively correlated to heat-knockdown time across populations. These results indicate that variation in heat-induced hormesis can not be considered as independent of heat-stress sensitivity (or heat-knockdown time) in populations of insects.

寿命中的热致兴奋是指由于早期暴露于轻度热应激而导致的寿命延长。在这里,我们在五个大规模交配种群中检测了热诱导的嗡嗡果蝇的兴奋,这些种群来自阿根廷西北部海拔202至1855米的五个野生种群。将5天大的苍蝇暴露在37.5°C下90分钟,以诱导兴奋及其在不同海拔种群中的可能变化。这种热处理大大延长了低地苍蝇的寿命,这些苍蝇只来自最耐热的种群。热诱导对寿命和热击倒时间(热应激敏感性)的影响均与原籍人口的海拔高度呈负相关。不同人群的荷尔蒙分泌与体温下降时间呈正相关。这些结果表明,在昆虫种群中,热诱导的兴奋性变化不能被认为与热应激敏感性(或热击倒时间)无关。
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引用次数: 0
Interaction effect of mutations in the genes (piwi and aub) of the Argonaute family and hobo transposons on the integral survival parameters of Drosophila melanogaster. Argonaute家族基因(piwi和aub)突变和hobo转座子对果蝇整体生存参数的相互作用。
IF 4.5 4区 医学 Q1 Nursing Pub Date : 2024-02-01 Epub Date: 2023-10-21 DOI: 10.1007/s10522-023-10062-x
Elena Yushkova

The Argonaute family genes (piwi and aub) involved in the production of small RNAs are responsible for the regulation of many cellular processes, including the suppression of genome instability, modulation of gene activity, and transposable elements. Dysfunction of these genes and the associated activation of transposable elements adversely affect reproductive development and quality of life. The role of transposons in contrast to retrotransposons and their interaction with genes of the Argonaute family in aging processes have not been studied. This study considers a scenario in which the piwi and aub genes in the presence of functional hobo transposons can modify the effects from the level of DNA damage to lifespan. The simultaneous presence of mutation (piwi or aub) and hobo (regardless of size) in the genome has practically no effect or (less often) leads to a decrease in the level of DNA damage in ovarian cells. A high level of sterility and low ovarian reserve were noted mainly with a combination of mutations and full-sized hobo elements. The combination of these two genetic factors negatively affects the fertility of young females and embryonic survival. Isolated cases of restoration of reproductive functions with age were noted but only in females that had low fertility in the early period of life. The presence of hobo transposons contributed to an increase in the lifespan of both mutant and non-mutant females. Dysfunction of the piwi and aub genes (without hobo) can reduce the lifespan of both sexes. Together, each mutation and hobo transposons act antagonistically/additively (in females) and synergistically/antagonistically (in males) to change the lifespan. In parameters of locus-specific instability, hobo activation was more pronounced in piwi gene dysfunction. The results obtained complement data on the study of new functions of Argonaute family genes and their interactions with transposable elements in the aging process.

参与小RNA产生的Argonaute家族基因(piwi和aub)负责调节许多细胞过程,包括抑制基因组不稳定性、调节基因活性和转座元件。这些基因的功能障碍和相关的转座元件的激活对生殖发育和生活质量产生不利影响。转座子相对于逆转录转座子的作用及其与Argonaute家族基因在衰老过程中的相互作用尚未得到研究。这项研究考虑了一种情况,即在功能性hobo转座子存在的情况下,piwi和aub基因可以改变DNA损伤水平对寿命的影响。基因组中突变(piwi或aub)和hobo(无论大小)的同时存在实际上没有影响,或者(很少)导致卵巢细胞中DNA损伤水平的降低。高水平的不育和低卵巢储备主要是由突变和全尺寸的hobo元件组合引起的。这两种遗传因素的结合对年轻女性的生育能力和胚胎存活产生了负面影响。注意到生殖功能随年龄恢复的孤立病例,但仅发生在生命早期生育率低的女性身上。hobo转座子的存在有助于增加突变和非突变雌性的寿命。piwi和aub基因的功能障碍(没有hobo)会缩短两性的寿命。每种突变和hobo转座子加在一起(在雌性中)和协同/拮抗(在雄性中)作用,以改变寿命。在位点特异性不稳定的参数中,hobo激活在piwi基因功能障碍中更为明显。该结果获得了Argonaute家族基因新功能及其在衰老过程中与转座元件相互作用研究的补充数据。
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引用次数: 0
AMPK signaling inhibits the differentiation of myofibroblasts: impact on age-related tissue fibrosis and degeneration. AMPK信号抑制肌成纤维细胞分化:对年龄相关组织纤维化和变性的影响。
IF 4.5 4区 医学 Q1 Nursing Pub Date : 2024-02-01 Epub Date: 2023-11-02 DOI: 10.1007/s10522-023-10072-9
Antero Salminen

Disruption of the extracellular matrix (ECM) and an accumulation of fibrotic lesions within tissues are two of the distinctive hallmarks of the aging process. Tissue fibroblasts are mesenchymal cells which display an impressive plasticity in the regulation of ECM integrity and thus on tissue homeostasis. Single-cell transcriptome studies have revealed that tissue fibroblasts exhibit a remarkable heterogeneity with aging and in age-related diseases. Excessive stress and inflammatory insults induce the differentiation of fibroblasts into myofibroblasts which are fusiform contractile cells and abundantly secrete the components of the ECM and proteolytic enzymes as well as many inflammatory mediators. Detrimental stresses can also induce the transdifferentiation of certain mesenchymal and myeloid cells into myofibroblasts. Interestingly, many age-related stresses, such as oxidative and endoplasmic reticulum stresses, ECM stiffness, inflammatory mediators, telomere shortening, and several alarmins from damaged cells are potent inducers of myofibroblast differentiation. Intriguingly, there is convincing evidence that the signaling pathways stimulated by the AMP-activated protein kinase (AMPK) are potent inhibitors of myofibroblast differentiation and accordingly AMPK signaling reduces fibrotic lesions within tissues, e.g., in age-related cardiac and pulmonary fibrosis. AMPK signaling is not only an important regulator of energy metabolism but it is also able to control cell fate determination and many functions of the immune system. It is known that AMPK signaling can delay the aging process via an integrated signaling network. AMPK signaling inhibits myofibroblast differentiation, e.g., by suppressing signaling through the TGF-β, NF-κB, STAT3, and YAP/TAZ pathways. It seems that AMPK signaling can alleviate age-related tissue fibrosis and degeneration by inhibiting the differentiation of myofibroblasts.

细胞外基质(ECM)的破坏和组织内纤维化病变的积聚是衰老过程的两个显著特征。组织成纤维细胞是间充质细胞,在ECM完整性的调节中表现出令人印象深刻的可塑性,从而影响组织稳态。单细胞转录组研究表明,组织成纤维细胞在衰老和与年龄相关的疾病中表现出显著的异质性。过度的压力和炎症损伤诱导成纤维细胞分化为肌成纤维细胞,肌成纤维纤维细胞是梭形收缩细胞,大量分泌ECM和蛋白水解酶的成分以及许多炎症介质。破坏性应激也可以诱导某些间充质细胞和骨髓细胞转分化为肌成纤维细胞。有趣的是,许多与年龄相关的应激,如氧化应激和内质网应激、ECM硬度、炎症介质、端粒缩短和损伤细胞的一些危言耸听,都是肌成纤维细胞分化的有效诱导剂。有趣的是,有令人信服的证据表明,AMP活化蛋白激酶(AMPK)刺激的信号通路是肌成纤维细胞分化的有效抑制剂,因此AMPK信号减少了组织内的纤维化病变,例如,在年龄相关的心脏和肺纤维化中。AMPK信号传导不仅是能量代谢的重要调节因子,而且能够控制细胞命运的决定和免疫系统的许多功能。众所周知,AMPK信令可以通过集成信令网络延迟老化过程。AMPK信号传导抑制肌成纤维细胞分化,例如通过抑制TGF-β、NF-κB、STAT3和YAP/TAZ途径的信号传导。AMPK信号传导似乎可以通过抑制肌成纤维细胞的分化来减轻与年龄相关的组织纤维化和变性。
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引用次数: 0
Disrupted HSF1 regulation in normal and exceptional brain aging. 正常和异常脑衰老过程中的 HSF1 调节紊乱
IF 4.5 4区 医学 Q1 Nursing Pub Date : 2024-02-01 Epub Date: 2023-09-14 DOI: 10.1007/s10522-023-10063-w
Rachana Trivedi, Bailey Knopf, Sharlene Rakoczy, Gunjan D Manocha, Holly Brown-Borg, Donald A Jurivich

Brain aging is a major risk factor for cognitive diseases such as Alzheimer's disease (AD) and vascular dementia. The rate of aging and age-related pathology are modulated by stress responses and repair pathways that gradually decline with age. However, recent reports indicate that exceptional longevity sustains and may even enhance the stress response. Whether normal and exceptional aging result in either attenuated or enhanced stress responses across all organs is unknown. This question arises from our understanding that biological age differs from chronological age and evidence that the rate of aging varies between organs. Thus, stress responses may differ between organs and depend upon regenerative capacity and ability to manage damaged proteins and proteotoxicity. To answer these questions, we assessed age-dependent changes in brain stress responses with normally aged wild type and long-lived Dwarf mice. Results from this study show that normal aging unfavorably impacts activation of the brain heat shock (HS) axis with key changes noted in the transcription factor, HSF1, and its regulation. Exceptional aging appears to preserve and strengthen many elements of HSF1 activation in the brain. These results support the possibility that reconstitution of aging brain stress responses requires a multi-factorial approach that addresses HSF1 protein levels, its DNA binding, and regulatory elements such as phosphorylation and protein interactions.

大脑老化是阿尔茨海默病(AD)和血管性痴呆等认知疾病的主要风险因素。衰老的速度和与年龄相关的病理变化受应激反应和修复途径的调节,而应激反应和修复途径会随着年龄的增长而逐渐衰退。然而,最近的报告表明,超常的长寿会维持甚至增强应激反应。正常衰老和超常衰老是否会导致所有器官的应激反应减弱或增强,目前尚不清楚。这个问题源于我们对生物年龄不同于计时年龄的理解,以及不同器官衰老速度不同的证据。因此,不同器官的应激反应可能不同,并取决于再生能力以及管理受损蛋白质和蛋白质毒性的能力。为了回答这些问题,我们用正常衰老的野生型小鼠和长寿侏儒小鼠评估了大脑应激反应随年龄的变化。研究结果表明,正常衰老对大脑热休克(HS)轴的激活有不利影响,转录因子 HSF1 及其调控发生了关键变化。异常衰老似乎保留并加强了大脑中激活 HSF1 的许多要素。这些结果支持这样一种可能性,即重建衰老大脑的应激反应需要一种多因素方法,以解决 HSF1 蛋白水平、其 DNA 结合以及磷酸化和蛋白质相互作用等调控要素的问题。
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引用次数: 0
Gut microbiota influence frailty syndrome in older adults: mechanisms and therapeutic strategies. 肠道微生物群对老年人虚弱综合征的影响:机制与治疗策略。
IF 4.5 4区 医学 Q1 Nursing Pub Date : 2024-02-01 Epub Date: 2023-12-27 DOI: 10.1007/s10522-023-10082-7
Xiao-Ming Wang, Lu Fan, Chen-Chen Meng, Yun-Jiao Wang, Li-E Deng, Zhuo Yuan, Jun-Ping Zhang, Yan-Yang Li, Shi-Chao Lv

Frailty syndrome denotes a decreased capacity of the body to maintain the homeostasis and stress of the internal environment, which simultaneously increases the risk of adverse health outcomes in older adults, including disability, hospitalization, falls, and death. To promote healthy aging, we should find strategies to cope with frailty. However, the pathogenesis of frailty syndrome is not yet clear. Recent studies have shown that the diversity, composition, and metabolites of gut microbiota significantly changed in older adults with frailty. In addition, several frailty symptoms were alleviated by adjusting gut microbiota with prebiotics, probiotics, and symbiosis. Therefore, we attempt to explore the pathogenesis of frailty syndrome in older people from gut microbiota and summarize the existing interventions for frailty syndrome targeting gut microbiota, with the aim of providing timely and necessary interventions and assistance for older adults with frailty.

虚弱综合征是指机体维持体内平衡和内环境压力的能力下降,这同时增加了老年人出现不良健康后果的风险,包括残疾、住院、跌倒和死亡。为了促进健康老龄化,我们应该找到应对虚弱的策略。然而,虚弱综合征的发病机理尚不清楚。最近的研究表明,患有虚弱症的老年人肠道微生物群的多样性、组成和代谢物发生了显著变化。此外,通过使用益生菌、益生菌和共生菌调整肠道微生物群,一些虚弱症状得到了缓解。因此,我们试图从肠道微生物区系探讨老年人虚弱综合征的发病机制,并总结现有的针对肠道微生物区系的虚弱综合征干预措施,以期为患有虚弱综合征的老年人提供及时、必要的干预和帮助。
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引用次数: 0
Seven knowledge gaps in modern biogerontology. 现代生物老年学的七大知识空白。
IF 4.5 4区 医学 Q1 Nursing Pub Date : 2024-02-01 DOI: 10.1007/s10522-023-10089-0
Suresh I S Rattan

About a year ago, members of the editorial board of Biogerontology were requested to respond to a query by the editor-in-chief of the journal as to what one question within their field of ageing research still needs to be asked and answered. This editorial is inspired by the wide range and variety of questions, ideas, comments and suggestions received in response to that query. The seven knowledge gaps identified in this article are arranged into three main categories: evolutionary aspects of longevity, biological survival and death aspects, and heterogeneity in the progression and phenotype of ageing. This is not an exhaustive and exclusive list, and may be modified and expanded. Implications of these knowledge gaps, especially in the context of ongoing attempts to develop effective interventions in ageing and longevity are also discussed.

大约一年前,《生物老年学》(Biogerontology)编辑部的成员被要求回答该杂志主编提出的一个问题,即在他们的老龄化研究领域中还有什么问题需要提出和回答。这篇社论的灵感来源于我们收到的各种各样的问题、想法、评论和建议。本文确定的七个知识缺口分为三大类:长寿的进化方面、生物生存和死亡方面以及老龄化进程和表型的异质性。这并不是一份详尽无遗的清单,可以进行修改和扩充。此外,还讨论了这些知识差距的影响,特别是在目前试图制定有效干预老龄化和长寿的背景下。
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引用次数: 0
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Biogerontology
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