bims-longev 2023-05-14 papers

bims-longev

Biomed News

on Longevity

Issue of 2023–05–14
twelve papers selected by
Andreea Nitescu

Probiotic Limosilactobacillus Reuteri (Lactobacillus Reuteri) Extends the Lifespan of Drosophila Melanogaster through Insulin/IGF-1 Signaling.
A Review on the Efficacy of Plant-derived Bio-active Compounds Curcumin and Aged Garlic Extract in Modulating Cancer and Age-related Diseases
Devo-Aging: Intersections Between Development and Aging.
From mitochondria to sarcopenia: role of 17β-estradiol and testosterone.
Advances in Plant Polysaccharides as Antiaging Agents: Effects and Signaling Mechanisms.
Blood Biomarkers for Healthy Aging.
The circadian clock, aging and its implications in cancer.
Autophagy and mitophagy: physiological implications in kidney inflammation and diseases.
Can Iron and Polyunsaturated Fatty Acid Supplementation Induce Ferroptosis?
Bacterial induction of B cell senescence promotes age-related changes in the gut microbiota.
New Insights into Calorie Restriction Induced Bone Loss.
Sebacic acid as a potential age-related biomarker of liver aging: evidence linking mice and human.

Aging Dis. 2023 02 04.

Probiotic Limosilactobacillus Reuteri (Lactobacillus Reuteri) Extends the Lifespan of Drosophila Melanogaster through Insulin/IGF-1 Signaling.

Hye-Yeon Lee, Ji-Hyeon Lee, Seung Hyung Kim, Su-Yeon Jo, Kyung-Jin Min.

The term probiotic refers to bacteria that provide a beneficial effect to the host. Limosilactobacillus reuteri (Lactobacillus reuteri) is a probiotic isolated from human breast milk. Although L. reuteri has antimicrobial and anti-inflammatory activities occasionally linked to anti-aging effects, there are no reports of the effects of L. reuteri on longevity. This study evaluated the anti-aging effects of L. reuteri on the lifespan and physiology of Drosophila melanogaster. L. reuteri increased the mean lifespan of fruit flies significantly without reducing the reproductive output, food intake, or locomotor activity. Furthermore, the data suggested that the longevity effect of L. reuteri is mediated by the reduction of the insulin/IGF-1 signaling pathway and the action of reuterin, an antimicrobial compound produced by L. reuteri. These results show that L. reuteri can be used as a probiotic that acts as a dietary restriction mimetic with anti-aging effects.

DOI: https://doi.org/10.14336/AD.2023.0122
Curr Rev Clin Exp Pharmacol. 2023 05 04.

A Review on the Efficacy of Plant-derived Bio-active Compounds Curcumin and Aged Garlic Extract in Modulating Cancer and Age-related Diseases

Diptimayee Das, Kanchan M, Abhijit Mitra, Y Zaky Mohamed, Surajit Pathak, Antara Banerjee.

  Aging is a process characterized by accumulating degenerative changes resulting in the death of an organism. Aging is mediated by various pathways that are directly linked to the individual's lifespan and are shunted for many age-related diseases. Many strategies for alleviating age-related diseases have been studied, which can target cells and molecules. Modern drugs such as Metformin, Rapamycin, and other drugs are used to reduce the effects of age-related diseases. Despite their beneficial activity, they possess some side effects which can limit their applications, mainly in older adults. Natural phytochemicals which have anti-aging activities have been studied by many researchers from a broader aspect and suggested that plant-based compounds can be a possible, direct, and practical way to treat age-related diseases which has enormous anti-aging activity. Also, studies indicated that the synergistic action of phytochemicals might enhance the biological effect rather than the individual or summative effects of natural compounds. Curcumin has an antioxidant property and is an effective scavenger of reactive oxygen species. Curcumin also has a beneficial role in many age-related diseases like diabetes, cardiovascular disease, neurological disorder, and cancer. Aged garlic extracts are also another bioactive component that has high antioxidant properties. Many studies demonstrated aged garlic extract, which has high antioxidant properties, could play a significant role in anti-aging and age-related diseases. The synergistic effect of these compounds can decrease the requirement of doses of a single drug, thus reducing its side effects caused by increased concentration of the single drug.

Keywords:  Age related disease; Aged garlic extract.; Aged garlic extractAging; Aging; Cancer; Curcumin

DOI:  https://doi.org/10.2174/2772432819666230504093227
Geroscience. 2023 May 09.

Devo-Aging: Intersections Between Development and Aging.

Carlos Giovanni Silva-García.

  There are two fundamental questions in developmental biology. How does a single fertilized cell give rise to a whole body? and how does this body later produce progeny? Synchronization of these embryonic and postembryonic developments ensures continuity of life from one generation to the next. An enormous amount of work has been done to unravel the molecular mechanisms behind these processes, but more recently, modern developmental biology has been expanded to study development in wider contexts, including regeneration, environment, disease, and even aging. However, we have just started to understand how the mechanisms that govern development also regulate aging. This review discusses examples of signaling pathways involved in development to elucidate how their regulation influences healthspan and lifespan. Therefore, a better knowledge of developmental signaling pathways stresses the possibility of using them as innovative biomarkers and targets for aging and age-related diseases.

Keywords:  Age-related diseases; Aging; Development; Environment; Epigenetics; FGF; Hedgehog; Hippo; IIS; TGF-b; Wnt; mTOR

DOI:  https://doi.org/10.1007/s11357-023-00809-2
Front Endocrinol (Lausanne). 2023 ;14 1156583

From mitochondria to sarcopenia: role of 17β-estradiol and testosterone.

Xu Tian, Shujie Lou, Rengfei Shi.

  Sarcopenia, characterized by a loss of muscle mass and strength with aging, is prevalent in older adults. Although the exact mechanisms underlying sarcopenia are not fully understood, evidence suggests that the loss of mitochondrial integrity in skeletal myocytes has emerged as a pivotal contributor to the complex etiology of sarcopenia. Mitochondria are the primary source of ATP production and are also involved in generating reactive oxygen species (ROS), regulating ion signals, and initiating apoptosis signals in muscle cells. The accumulation of damaged mitochondria due to age-related impairments in any of the mitochondrial quality control (MQC) processes, such as proteostasis, biogenesis, dynamics, and mitophagy, can contribute to the decline in muscle mass and strength associated with aging. Interestingly, a decrease in sex hormones (e.g., 17β-estradiol and testosterone), which occurs with aging, has also been linked to sarcopenia. Indeed, 17β-estradiol and testosterone targeted mitochondria and exhibited activities in regulating mitochondrial functions. Here, we overview the current literature on the key mechanisms by which mitochondrial dysfunction contribute to the development and progression of sarcopenia and the potential modulatory effects of 17β-estradiol and testosterone on mitochondrial function in this context. The advance in its understanding will facilitate the development of potential therapeutic agents to mitigate and manage sarcopenia.

Keywords:  17β-estradiol; aging; mitochondria; sarcopenia; skeletal muscle; testosterone

DOI:  https://doi.org/10.3389/fendo.2023.1156583
J Agric Food Chem. 2023 May 08.

Advances in Plant Polysaccharides as Antiaging Agents: Effects and Signaling Mechanisms.

Rou Deng, Fang Wang, Luanfeng Wang, Ling Xiong, Xinchun Shen, Haizhao Song.

  Aging refers to the gradual physiological changes that occur in an organism after reaching adulthood, resulting in senescence and a decline in biological functions, ultimately leading to death. Epidemiological evidence shows that aging is a driving factor in the developing of various diseases, including cardiovascular diseases, neurodegenerative diseases, immune system disorders, cancer, and chronic low-grade inflammation. Natural plant polysaccharides have emerged as crucial food components in delaying the aging process. Therefore, it is essential to continuously investigate plant polysaccharides as potential sources of new pharmaceuticals for aging. Modern pharmacological research indicates that plant polysaccharides can exert antiaging effects by scavenging free radicals, increasing telomerase activity, regulating apoptosis, enhancing immunity, inhibiting glycosylation, improving mitochondrial dysfunction regulating gene expression, activating autophagy, and modulating gut microbiota. Moreover, the antiaging activity of plant polysaccharides is mediated by one or more signaling pathways, including IIS, mTOR, Nrf2, NF-κB, Sirtuin, p53, MAPK, and UPR signaling pathways. This review summarizes the antiaging properties of plant polysaccharides and signaling pathways participating in the polysaccharide-regulating aging process. Finally, we discuss the structure-activity relationships of antiaging polysaccharides.

Keywords:  antiaging effects; polysaccharides; signaling mechanisms; structure−activity relationships

DOI:  https://doi.org/10.1021/acs.jafc.3c00493
Gerontology. 2023 Apr 25.

Blood Biomarkers for Healthy Aging.

Ceereena Ubaida-Mohien, Toshiko Tanaka, Qu Tian, Zenobia Moore, Ruin Moaddel, Nathan Basisty, Eleanor M Simonsick, Luigi Ferrucci.

Measuring the abundance of biological molecules and their chemical modifications in blood and tissues has been the cornerstone of research and medical diagnoses for decades. Although the number and variety of molecules that can be measured have expanded exponentially, the blood biomarkers routinely assessed in medical practice remain limited to a few dozen, which have not substantially changed over the last 30-40 years. The discovery of novel biomarkers would allow, for example, risk stratification or monitoring of disease progression or the effectiveness of treatments and interventions, improving clinical practice in myriad ways. In this review, we combine the biomarker discovery concept with geroscience. Geroscience bridges aging research and translation to clinical applications by combining the framework of medical gerontology with high-technology medical research. With the development of geroscience and the rise of blood biomarkers, there has been a paradigm shift from disease prevention and cure to promoting health and healthy aging. New -omic technologies have played a role in the development of blood biomarkers, including epigenetic, proteomic, metabolomic, and lipidomic markers, which have emerged as correlates or predictors of health status, from disease and exceptional health.

DOI: https://doi.org/10.1159/000530795
Neoplasia. 2023 Jul;pii: S1476-5586(23)00029-5. [Epub ahead of print]41 100904

The circadian clock, aging and its implications in cancer.

Abdol-Hossein Rezaeian, Fabin Dang, Wenyi Wei.

Circadian clock orchestrates the intergenic biochemical, physiological and behavioral changes to form an approximate 24h oscillation through the transcription-translation feedback loop (TTFL). Mechanistically, a heterodimer of transcriptional activator formed by BMAL1 and CLOCK, governs the expression of its transcriptional repressors, CRY, PER and REV-ERBα/β proteins, thereby controlling more than 50 % of protein encoding genes in human. There is also increasing evidence showing that tumor microenvironment can disrupt specific clock gene functions to facilitate tumorigenesis. Although there is great progress in understanding the molecular mechanisms of the circadian clock, aging and cancer, elucidating their complex relationships among these processes remains challenging. Herein, the optimization of the chronochemotherapy regimen has not been justified yet for treatment of cancer. Here, we discuss the hypothesis of relocalization of chromatin modifiers (RCM) along with function(s) of the circadian rhythm on aging and carcinogenesis. We will also introduce the function of the chromatin remodeling as a new avenue for rejuvenation of competent tissues to combat aging and cancer.

DOI: https://doi.org/10.1016/j.neo.2023.100904
Am J Physiol Renal Physiol. 2023 May 11.

Autophagy and mitophagy: physiological implications in kidney inflammation and diseases.

Divya Bhatia, Mary E Choi.

  Autophagy is a ubiquitous intracellular cytoprotective quality control program that maintains cellular homeostasis by recycling superfluous cytoplasmic components (lipid droplets, protein, or glycogen aggregates) and invading pathogens. Mitophagy is a selective form of autophagy that by recycling damaged mitochondrial material, which can extracellularly act as damage-associated molecular patterns, prevents their release. Autophagy and mitophagy are indispensable for the maintenance of kidney homeostasis and exert crucial functions during both physiological and disease conditions. Impaired autophagy and mitophagy can negatively impact the pathophysiological state and promote its progression. Autophagy helps in maintaining structural integrity of the kidney. Mitophagy-mediated mitochondrial quality control is explicitly critical for regulating cellular homeostasis in the kidney. Both autophagy and mitophagy attenuate the inflammatory responses in the kidney. Accumulating body of evidence highlights that persistent kidney injury-induced oxidative stress can contribute to dysregulated autophagic and mitophagic responses, and cell death. Autophagy and mitophagy also communicate with programmed cell death pathways (apoptosis, necroptosis), and play important roles in cell survival by preventing nutrient deprivation and regulating oxidative stress. Autophagy and mitophagy are activated in the kidney after acute injury. However, their aberrant hyperactivation can be deleterious and cause tissue damage. The findings on the functions of autophagy and mitophagy in various models of chronic kidney disease are heterogenous, and cell type and context-specific dependent. In this review, we discuss the roles of autophagy and mitophagy in the kidney in regulating inflammatory responses, and during various pathological manifestations.

Keywords:  AKI; Autophagy; CKD; Kidney inflammation; Mitophagy

DOI:  https://doi.org/10.1152/ajprenal.00012.2023
Cell Physiol Biochem. 2023 Feb 15. 57(1): 34-48

Can Iron and Polyunsaturated Fatty Acid Supplementation Induce Ferroptosis?

Elena G Novoselova, Sergey M Lunin, Maxim O Khrenov, Olga V Glushkova, Tatiana V Novoselova, Svetlana B Parfenyuk.

  This minireview discusses the very important biomedical problem of treating type 2 diabetes mellitus (T2D). T2D accounts for more than 90% of the total number of diagnosed cases of diabetes mellitus and can result from aging, inflammation, obesity and β-cell senescence. The main symptom of both T2D and type 1 diabetes (T1D) is an increase in blood glucose concentration. While T1D is insulin-dependent and is associated with the destruction of pancreatic β-cells, T2D does not require lifelong insulin administration. In this case, pancreatic β-cells are not destroyed, but their functional activity is deregulated. In T2D, metabolic stress increases the number of senescent β-cells while impairing glucose tolerance. The potential paracrine effects of senescent β-cells highlight the importance of the β-cell senescenceassociated secretory phenotype (SASP) in driving metabolic dysfunction. We believe that the main reason for the deregulation of the functional activity of pancreatic β-cells in T2D is associated with their "aging" or senescence, which may be induced by various stressors. We propose the use of peroxiredoxin 6 as a new senolytic drug, and the role of β-cell senescence in the development of T2D is discussed in this review.

Keywords:  Type 2 diabetes mellitus ; Senescent β-cells ; Aging ; Inflammation ; Obesity

DOI:  https://doi.org/10.33594/000000606
Nat Cell Biol. 2023 May 11.

Bacterial induction of B cell senescence promotes age-related changes in the gut microbiota.

Shimpei Kawamoto, Ken Uemura, Nozomi Hori, Lena Takayasu, Yusuke Konishi, Kazutaka Katoh, Tomonori Matsumoto, Masae Suzuki, Yusuke Sakai, Tatsuyuki Matsudaira, Takahiro Adachi, Naoko Ohtani, Daron M Standley, Wataru Suda, Shinji Fukuda, Eiji Hara.

The elucidation of the mechanisms of ageing and the identification of methods to control it have long been anticipated. Recently, two factors associated with ageing-the accumulation of senescent cells and the change in the composition of gut microbiota-have been shown to play key roles in ageing. However, little is known about how these phenomena occur and are related during ageing. Here we show that the persistent presence of commensal bacteria gradually induces cellular senescence in gut germinal centre B cells. Importantly, this reduces both the production and diversity of immunoglobulin A (IgA) antibodies that target gut bacteria, thereby changing the composition of gut microbiota in aged mice. These results have revealed the existence of IgA-mediated crosstalk between the gut microbiota and cellular senescence and thus extend our understanding of the mechanism of gut microbiota changes with age, opening up possibilities for their control.

DOI: https://doi.org/10.1038/s41556-023-01145-5
Endocrinol Metab (Seoul). 2023 Apr;38(2): 203-213

New Insights into Calorie Restriction Induced Bone Loss.

Linyi Liu, Clifford J Rosen.

  Caloric restriction (CR) is now a popular lifestyle choice due to its ability in experimental animals to improve lifespan, reduce body weight, and lessen oxidative stress. However, more and more emerging evidence suggests this treatment requires careful consideration because of its detrimental effects on the skeletal system. Experimental and clinical studies show that CR can suppress bone growth and raise the risk of fracture, but the specific mechanisms are poorly understood. Reduced mechanical loading has long been thought to be the primary cause of weight loss-induced bone loss from calorie restriction. Despite fat loss in peripheral depots with calorie restriction, bone marrow adipose tissue (BMAT) increases, and this may play a significant role in this pathological process. Here, we update recent advances in our understanding of the effects of CR on the skeleton, the possible pathogenic role of BMAT in CR-induced bone loss, and some strategies to mitigate any potential side effects on the skeletal system.

Keywords:  Bone and bones; Bone marrow adipose tissue; Caloric restriction; Exercise; Parathyroid hormone; Vitamin D

DOI:  https://doi.org/10.3803/EnM.2023.1673
J Gerontol A Biol Sci Med Sci. 2023 May 06. pii: glad121. [Epub ahead of print]

Sebacic acid as a potential age-related biomarker of liver aging: evidence linking mice and human.

Chen-Hua Huang, Wei-Ju Lee, Yi-Long Huang, Ting-Fen Tsai, Liang-Kung Chen, Chao-Hsiung Lin.

  The aging process is complicated and involves diverse organ dysfunction; furthermore, the biomarkers that are able to reflect biological aging are eagerly sought after in order to monitor the system-wide decline associated with the aging process. To address this, we performed a metabolomics analysis using a longitudinal cohort study from Taiwan (N=710) and established plasma metabolomic age using a machine learning algorithm. The resulting estimation of age acceleration among the older adults was found to be correlated with HOMA-insulin resistance. In addition, a sliding window analysis was used to investigate the undulating decrease in hexanoic and heptanoic acids that occurs among the older adults at different ages. A comparison of the metabolomic alterations associated with aging between humans and mice implied that ω-oxidation of medium chain fatty acids was commonly dysregulated in older subjects. Among these fatty acids, sebacic acid, an ω-oxidation product produced by the liver, was significantly decreased in the plasma of both older humans and aged mice. Notably, an increase in the production and consumption of sebacic acid within the liver tissue of aged mice was observed, along with an elevation of pyruvate-to-lactate conversion. Taken together, our study reveals that sebacic acid and metabolites of ω-oxidation are the common aging biomarkers in both humans and mice. The further analysis suggests that sebacic acid may play an energetic role to supporting the production of acetyl-CoA during liver aging, and thus its alteration in plasma concentration potentially reflects the aging process.

Keywords:  Human aging; Metabolomic age; Metabolomics; Plasma

DOI:  https://doi.org/10.1093/gerona/glad121