Aging-US

BUFFALO, NY- December 6, 2023 – A new #editorial paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Artificial intelligence for aging research in cancer drug development.”

Aging is a multifactorial and complex process associated with various diseases, including cancer. In light of the growing aging population, the need for effective cancer treatments is more significant than ever. Artificial intelligence (AI) is playing an increasingly crucial role in aging research and cancer drug development in revealing the critical drivers of outcomes among a wide range of intrinsic and extrinsic factors.

In recent years, the use of AI in aging research has been rapidly increasing, suggesting that AI-based analysis of healthcare data may enhance clinical care. In this new editorial, researchers Dorsa Shirini, Lawrence H. Schwartz and Laurent Dercle from Columbia University Medical Center provide an overview of the potential benefits as well as the technical caveats of adopting AI to help researchers identify new targets, develop more effective therapies, and accelerate the discovery process of drug development in the context of aging research.

“In this review, we discuss how we could leverage AI technologies to consider a patient’s unique aging profile and tailor cancer treatment more precisely to the individual. This approach would help optimize treatment outcomes, minimize treatment-related risks, and improve the overall quality of care for patients, considering the complex interplay between aging and cancer treatment response.”

DOI - https://doi.org/10.18632/aging.204914

Corresponding authors - Laurent Dercle - [email protected]

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Keywords - aging, artificial intelligence, cancer research

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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BUFFALO, NY- December 5, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Contribution of membrane raft redox signalling to visfatin-induced inflammasome activation and podocyte injury.”

The number of obese patients with end stage renal disease has increased significantly worldwide in the last few decades. Obesity results in an increased risk for chronic kidney diseases like diabetes and hypertension which consequently result in chronic kidney disease or even end-stage renal disease. However, the exact mechanism of how obesity increases the advancement of chronic kidney disease is still uncertain.

Recently, researchers Saisudha Koka, Sreenidhi Surineni, Gurinder Bir Singh, and Krishna M. Boini from the University of Houston, Texas A&M University and the University of California Riverside have shown that adipokine visfatin-induced NLRP3 inflammasome activation contributes to podocyte injury. However, the molecular mechanisms of how visfatin induces the Nlrp3 inflammasome activation and podocyte damage is still unknown. The present study tested whether the membrane raft (MR) redox signaling pathway plays a central role in visfatin-induced NLRP3 inflammasomes formation and activation in podocytes.

“In this study, it is proposed that visfatin induces the NLRP3 inflammasome activation in podocytes, leading to glomerular inflammatory injury in the kidney and the development of CKD, may be primarily driven by NADPH oxidase-mediated membrane raft redox signalling.”

Upon visfatin stimulation, an aggregation of NADPH oxidase subunits, gp91phox and p47phox, was observed in the MR clusters, forming an MR redox signaling platform in podocytes. The formation of this signaling platform was blocked by prior treatment with MR disruptor MCD or NADPH oxidase inhibitor DPI. In addition, visfatin stimulation significantly increased the colocalization of Nlrp3 with Asc or Nlrp3 with caspase-1, IL-β production, cell permeability in podocytes compared to control cells.

Pretreatment with MCD, DPI, WEHD significantly abolished the visfatin-induced colocalization of NLRP3 with Asc or NLRP3 with caspase-1, IL-1β production and cell permeability in podocytes. Furthermore, Immunofluorescence analysis demonstrated that visfatin treatment significantly decreased the podocin and nephrin expression (podocyte damage) and prior treatments with DPI, WEHD, MCD attenuated this visfatin-induced podocin and nephrin reduction. In conclusion, their results suggest that visfatin stimulates membrane raft clustering in the membrane of podocytes to form redox signaling platforms by aggregation and activation of NADPH oxidase subunits enhancing O2·− production, leading to NLRP3 inflammasome activation in podocytes and ultimate podocyte injury.

“Through experiments conducted on cultured podocytes, we have demonstrated, for the first time that membrane raft-associated redox signalling is essential for the NLRP3 inflammasomes assembly and activation in response to visfatin, subsequently resulting in podocyte dysfunction and injury. These findings shed light on a novel mechanism underlying inflammasome activation and injury of podocytes triggered by visfatin.”

DOI - https://doi.org/10.18632/aging.205243

Corresponding author - Krishna M. Boini - [email protected]

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BUFFALO, NY- November 30, 2023 – A new #researchpaper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 22, entitled, “Chronological aging impacts abundance, function and microRNA content of extracellular vesicles produced by human epidermal keratinocytes.”

The disturbance of intercellular communication is one of the hallmarks of aging. In their new study, researchers Taku Nedachi, Christelle Bonod, Julie Rorteau, Wafae Chinoune, Yuri Ishiuchi, Sandrine Hughes, Benjamin Gillet, Nicolas Bechetoille, Dominique Sigaudo-Roussel, and Jérôme Lamartine from the University of Lyon, Toyo University and Gattefossé SAS aimed to clarify the impact of chronological aging on extracellular vesicles (EVs), a key mode of communication in mammalian tissues.

“The present study was therefore conducted to elucidate whether the characteristics of EVs released from cultured human keratinocytes can be modulated during aging process.”

The researchers focused on epidermal keratinocytes, the main cells of the outer protective layer of the skin which is strongly impaired in the skin of elderly. EVs were purified from conditioned medium of primary keratinocytes isolated from infant or aged adult skin. A significant increase of the relative number of EVs released from aged keratinocytes was observed whereas their size distribution was not modified.

By small RNA sequencing, the researchers described a specific microRNA (miRNA) signature of aged EVs with an increase abundance of miR-30a, a key regulator of barrier function in human epidermis. EVs from aged keratinocytes were found to be able to reduce the proliferation of young keratinocytes, to impact their organogenesis properties in a reconstructed epidermis model and to slow down the early steps of skin wound healing in mice, three features observed in aged epidermis. This work reveals that intercellular communication mediated by EVs is modulated during aging process in keratinocytes and might be involved in the functional defects observed in aged skin.

“To conclude, we have shown here that aging modulates EVs abundance, function and microRNA content in human keratinocytes.”

DOI - https://doi.org/10.18632/aging.205245

Corresponding author - Jérôme Lamartine - [email protected]

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Keywords - aging, keratinocytes, microRNA, senescence, exosomes

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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BUFFALO, NY- November 28, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 21, entitled, “1,5-anhydro-D-fructose induces anti-aging effects on aging-associated brain diseases by increasing 5’-adenosine monophosphate-activated protein kinase activity via the peroxisome proliferator-activated receptor-γ co-activator-1α/brain-derived neurotrophic factor pathway.”

5’-Adenosine monophosphate-activated protein kinase (AMPK) is a metabolic sensor that serves as a cellular housekeeper; it also controls energy homeostasis and stress resistance. Thus, correct regulation of this factor can enhance health and survival. AMPK signaling may have a critical role in aging-associated brain diseases. Some in vitro studies have shown that 1,5-anhydro-D-fructose (1,5-AF) induces AMPK activation.

In this new study, researchers Kiyoshi Kikuchi, Shotaro Otsuka, Seiya Takada, Kazuki Nakanishi, Kentaro Setoyama, Harutoshi Sakakima, Eiichiro Tanaka, and Ikuro Maruyama from Kagoshima University investigated the effects of 1,5-AF on the AMPK/PGC-1α/BDNF pathway in multiple animal models of human aging-associated brain diseases.

“In the present study, we experimentally evaluated the effects of 1,5-AF on aging-associated brain diseases in vivo using an animal model of acute ischemic stroke (AIS), stroke-prone spontaneously hypertensive rats (SHRSPs), and the spontaneous senescence-accelerated mouse-prone 8 (SAMP8) model.”

In the AIS model, intraperitoneal injection of 1,5-AF reduced cerebral infarct volume, neurological deficits, and mortality. In SHRSPs, oral administration of 1,5-AF reduced blood pressure and prolonged survival. In the SAMP8 model, oral administration of 1,5-AF alleviated aging-related decline in motor cognitive function. Although aging reduced the expression levels of peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α) and brain-derived neurotrophic factor (BDNF), the researchers found that 1,5-AF activated AMPK, which led to upregulation of the PGC-1α/BDNF pathway.

“Our results suggest that 1,5-AF can induce endogenous neurovascular protection, potentially preventing aging-associated brain diseases. Clinical studies are needed to determine whether 1,5-AF can prevent aging-associated brain diseases.”

DOI - https://doi.org/10.18632/aging.205228

Corresponding authors - Kiyoshi Kikuchi - [email protected], and Ikuro Maruyama - [email protected]

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Keywords - aging, AMP-activated protein kinases, brain-derived neurotrophic factor, peroxisome proliferator-activated receptors, blood pressure

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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BUFFALO, NY- November 22, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 21, entitled, “Antibiotics that target mitochondria extend lifespan in C. elegans.”

Aging is a continuous degenerative process caused by a progressive decline of cell and tissue functions in an organism. It is induced by the accumulation of damage that affects normal cellular processes, ultimately leading to cell death. It has been speculated for many years that mitochondria play a key role in the aging process.

In this new study, researchers Gloria Bonuccelli, Darren R. Brooks, Sally Shepherd, Federica Sotgia, and Michael P. Lisanti from the University of Salford aimed to characterize the implications of mitochondria in aging using Caenorhabditis elegans (C. elegans) as an organismal model. The C. elegans were treated with a panel of mitochondrial inhibitors and assessed for survival.

“In our study, we assessed survival by evaluating worm lifespan, and we assessed aging markers by evaluating the pharyngeal muscle contraction, the accumulation of lipofuscin pigment and ATP levels.”

Their results show that treatment of worms with either doxycycline, azithromycin (inhibitors of the small and the large mitochondrial ribosomes, respectively), or a combination of both, significantly extended median lifespan of C. elegans, enhanced their pharyngeal pumping rate, reduced their lipofuscin content and their energy consumption (ATP levels), as compared to control untreated worms, suggesting an aging-abrogating effect for these drugs. Similarly, DPI, an inhibitor of mitochondrial complex I and II, was capable of prolonging the median lifespan of treated worms. On the other hand, subjecting worms to vitamin C, a pro-oxidant, failed to extend C. elegans lifespan and upregulated its energy consumption, revealing an increase in ATP level.

“Therefore, our longevity study reveals that mitochondrial inhibitors (i.e., mitochondria-targeting antibiotics) could abrogate aging and extend lifespan in C. elegans.”

DOI - https://doi.org/10.18632/aging.205229

Corresponding authors - Michael P. Lisanti - [email protected], and Federica Sotgia - [email protected]

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Keywords - aging, C. elegans, lifespan, lipofuscin, antibiotics, mitochondria, metabolism, DPI

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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BUFFALO, NY- November 16, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 21, entitled, “Parental age effect on the longevity and healthspan in Drosophila melanogaster and Caenorhabditis elegans.”

Several studies have investigated the effect of parental age on biological parameters such as reproduction, lifespan, and health; however, the results have been inconclusive, largely due to inter-species variation and/or modest effect sizes.

In their new study, researchers Camille Lenzi, Alexis Piat, Pascal Schlich, Judith Ducau, Jean-Claude Bregliano, Hugo Aguilaniu, and Anne Laurençon from the IM Projet, Caduceum, INRAE, IBDM, Instituto Serrapilheira, and Universite Claude Bernard-Lyon 1 examined the effect of parental age on the lifespan, reproductive capacity, and locomotor activity of genetic isogenic lines of the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster.

“We decided to investigate parental age impact on the lifespan of their progeny on selected genomes of flies and worms to gain insights on the molecular mechanisms at work.”

The researchers found that the progeny of successive generations of old parents had significantly shorter lifespans than the progeny of young parents in both species. Moreover, they investigated the fertility, fecundity, and locomotor activity of C. elegans. Interestingly, both the shorter lifespan and deteriorated healthspan of the progeny were significantly improved by switching to only one generation of younger parents.

“Collectively, these data demonstrate that the detrimental effect of older parental age on the longevity of the progeny can be reversed, suggesting the existence of a beneficial non–genetic mechanism.”

DOI - https://doi.org/10.18632/aging.205098

Corresponding author - Anne Laurençon - [email protected]

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Keywords - aging, life span, intergenerational plasticity, maternal effect, nematode, drosophila

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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BUFFALO, NY- November 15, 2023 – A new #researchpaper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 21, entitled, “Longitudinal characterization of behavioral, morphological and transcriptomic changes in a tauopathy mouse model.”

Neurodegenerative disorders, such as Alzheimer’s disease (AD), have the gradual onset of neurobiological changes preceding clinical diagnosis by decades. In their new study, researchers Qing Cao, Manasa Kumar, Allea Frazier, Jamal B. Williams, Shengkai Zhao, and Zhen Yan from the State University of New York at Buffalo’s Jacobs School of Medicine and Biomedical Sciences aimed to elucidate how brain dysfunction proceeds in neurodegenerative disorders.

“[...] we performed longitudinal characterization of behavioral, morphological, and transcriptomic changes in a tauopathy mouse model, P301S transgenic mice.”

P301S mice exhibited cognitive deficits as early as 3 months old, and deficits in social preference and social cognition at 5–6 months. They had a significant decrease of arborization in basal dendrites of hippocampal pyramidal neurons from 3 months and apical dendrites of PFC pyramidal neurons at 9 months. Transcriptomic analysis of genome-wide changes revealed the enrichment of synaptic gene upregulation at 3 months of age, while most of these synaptic genes were downregulated in PFC and hippocampus of P301S mice at 9 months. These time-dependent changes in gene expression may lead to progressive alterations of neuronal structure and function, resulting in the manifestation of behavioral symptoms in tauopathies.

“In conclusion, our longitudinal characterization of behavioral, morphological and transcriptomic changes in a tauopathy mouse model is to elucidate potential mechanisms that drive the progression of AD and related neurodegenerative disorders. Manipulation of key molecular players coupled with electrophysiological measurements of neuronal functions in future studies will help identify early intervention strategies for these diseases.”

DOI - https://doi.org/10.18632/aging.205057

Corresponding author - Zhen Yan - [email protected]

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Keywords - aging, Alzheimer’s disease, tau, cognitive behaviors, transcriptomic, neuronal morphology

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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BUFFALO, NY- November 14, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 20, entitled, “Alcohol consumption and epigenetic age acceleration across human adulthood.”

The alcohol-associated biological aging remains to be studied across adulthood. In their new study, researchers Mengyao Wang, Yi Li, Meng Lai, Drew R. Nannini, Lifang Hou, Roby Joehanes, Tianxiao Huan, Daniel Levy, Jiantao Ma, and Chunyu Liu from Boston University School of Public Health, Northwestern University Feinberg School of Medicine, National Institutes of Health, Framingham Heart Study, and Tufts University conducted linear regression analyses to investigate the associations between alcohol consumption and two DNA methylation-based biological age acceleration metrics in 3823 Framingham Heart Study participants (24–92 years and 53.8% women) adjusting for covariates.

“We also investigated whether the two epigenetic aging metrics mediated the association of alcohol consumption with hypertension.”

They found that higher long-term average alcohol consumption was significantly associated with biological age acceleration assessed by GrimAge acceleration (GAA) and PhenoAge acceleration (PAA) in middle-aged (45–64 years, n = 1866) and older (65–92 years, n = 1267) participants while not in young participants (24–44 years, n = 690). For example, one additional standard drink of alcohol (~14 grams of ethanol per day) was associated with a 0.71 ± 0.15-year (p = 2.1e-6) and 0.60 ± 0.18-year (p = 7.5e-4) increase in PAA in middle-aged and older participants, respectively, but the association was not significant in young participants (p = 0.23). One additional standard serving of liquor (~14 grams of ethanol) was associated with a greater increase in GAA (0.82-year, p = 4.8e-4) and PAA (1.45-year, p = 7.4e-5) than beer (GAA: 0.45-year, p = 5.2e-4; PAA: 0.48-year, p = 0.02) and wine (GAA: 0.51-year, p = 0.02; PAA: 0.91-year, p = 0.008) in middle-aged participant group.

“We observed that up to 28% of the association between alcohol consumption and hypertension was mediated by GAA or PAA in the pooled sample. Our findings suggest that alcohol consumption is associated with greater biological aging quantified by epigenetic aging metrics, which may mediate the association of alcohol consumption with quantitative traits, such as hypertension.”

DOI - https://doi.org/10.18632/aging.205153

Corresponding authors - Jiantao Ma - [email protected], and Chunyu Liu - [email protected]

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Keywords - aging, alcohol consumption, epigenetic aging, DNA methylation, hypertension

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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Pancreatic cancer is one of the deadliest forms of cancer, with a very low survival rate and limited treatment options. Understanding the molecular mechanisms that drive the development and progression of this disease is crucial for finding new ways to prevent and treat it. One of the key players in pancreatic cancer is the WNT signaling pathway, which regulates many aspects of cell growth, differentiation and survival. WNT signaling is often dysregulated in pancreatic cancer, leading to uncontrolled cell proliferation, invasion and resistance to therapy.

“The canonical WNT pathway is reportedly an essential protagonist in organ development as well as oncogenesis in multiple cancers.”

How does WNT signaling become so powerful in pancreatic cancer cells? In a new study, researchers Jing Wang, Dominik T. Koch, Felix O. Hofmann, Daniel Härtwig, Iris Beirith, Klaus Peter Janssen, Alexandr V. Bazhin, Hanno Niess, Jens Werner, Bernhard W. Renz, and Matthias Ilmer from Ludwig-Maximilians-University, University of Science and Technology of China, Technical University of Munich, and German Cancer Consortium revealed a novel role for a receptor called LGR6 in enhancing WNT signals in this disease. Their research paper was published on September 27, 2023, in Aging’s Volume 15, Issue 20, entitled, “WNT enhancing signals in pancreatic cancer are transmitted by LGR6.”

Full blog - https://aging-us.org/2023/11/how-a-receptor-boosts-wnt-signals-in-pancreatic-cancer/

Paper DOI - https://doi.org/10.18632/aging.205101

Corresponding author - Matthias Ilmer - [email protected]

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Keywords - aging, pancreatic ductal adenocarcinoma, WNT signaling, epithelial-mesenchymal transition, LGR6, cancer stem cells

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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BUFFALO, NY- November 8, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 20, entitled, “Tissue immunoexpression of IL-6 and IL-18 in aging men with BPH and MetS and their relationship with lipid parameters and gut microbiota-derived short chain fatty acids.”

Recent studies indicate that inflammation is one of the causes of the development of benign prostatic hyperplasia (BPH). Inflammation may result from past infections, metabolic disorders, but also from the state of functioning of the intestinal microbiota.

In this new study, researchers Weronika Ratajczak, Maria Laszczyńska, Aleksandra Rył, Barbara Dołęgowska, Olimpia Sipak, Ewa Stachowska, Marcin Słojewski, and Anna Lubkowska from Poland’s Pomeranian Medical University and State University of Applied Sciences aimed to assess whether the diagnostic lipid parameters for metabolic syndrome and short-chain fatty acids (SCFAs) are related to the immunoexpression of interleukins in prostate tissue with benign hyperplasia. The study involved 103 men with BPH, who were divided into two groups depending on the presence of MetS.

“We analysed tissue immunoexpression of two proinflammatory interleukins: IL-6, which is known to be involved in the development of BPH, and IL-18, which has not been analysed so far.”

The results of their study indicated that men with BPH + MetS in the stroma of the prostate have a significantly higher overall percentage of IL-6+ cells compared to men without MetS (p = 0.034). The analysis of IL-18 immunoexpression in prostate tissue indicated that in men with BPH + MetS, the glandular part of the prostate had a significantly higher percentage of cells with strong IL-18 expression (p = 0.040). They also noticed a relationship between tissue expression of IL-6 and IL-18 and lipid parameters (TG and HDL).

“We conclude that lipid disorders occurring in men with BPH increase inflammation in the prostate gland. Moreover, it has also been demonstrated for the first time that, indirectly, through SCFAs, the gut microbiota can act to prevent or create an inflammatory microenvironment in the prostate gland.”

DOI - https://doi.org/10.18632/aging.205091

Corresponding author - Anna Lubkowska - [email protected]

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Keywords - aging, benign prostatic hyperplasia (BPH), metabolic syndrome (MetS), lipids, interleukin 6 (IL-6), interleukin 18 (IL-18), short-chain fatty acids

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Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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