Inflammaging: The Immunology of Aging

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Cells cells	5.1	9.9	2012	17 Days	CHF 2700
Geriatrics geriatrics	2.1	3.3	2016	23.9 Days	CHF 1800
Immuno immuno	2.1	2.6	2021	26.8 Days	CHF 1000
International Journal of Molecular Sciences ijms	4.9	8.1	2000	16.8 Days	CHF 2900
Journal of Clinical Medicine jcm	3.0	5.7	2012	16 Days	CHF 2600

15 pages, 2177 KiB

Open AccessArticle

The Inflammasome Adaptor Protein ASC in Plasma as a Biomarker of Early Cognitive Changes

by Brianna Cyr, Rosie Curiel Cid, David Loewenstein, Regina T. Vontell, W. Dalton Dietrich, Robert W. Keane and Juan Pablo de Rivero Vaccari

Int. J. Mol. Sci. 2024, 25(14), 7758; https://doi.org/10.3390/ijms25147758 - 16 Jul 2024

Cited by 1 | Viewed by 1660

Abstract

Dementia is a group of symptoms including memory loss, language difficulties, and other types of cognitive and functional impairments that affects 57 million people worldwide, with the incidence expected to double by 2040. Therefore, there is an unmet need to develop reliable biomarkers [...] Read more.

Dementia is a group of symptoms including memory loss, language difficulties, and other types of cognitive and functional impairments that affects 57 million people worldwide, with the incidence expected to double by 2040. Therefore, there is an unmet need to develop reliable biomarkers to diagnose early brain impairments so that emerging interventions can be applied before brain degeneration. Here, we performed biomarker analyses for apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), and amyloid-β 42/40 (Aβ_42/40) ratio in the plasma of older adults. Participants had blood drawn at baseline and underwent two annual clinical and cognitive evaluations. The groups tested either cognitively normal on both evaluations (N_N), cognitively normal year 1 but cognitively impaired year 2 (N_I), or cognitively impaired on both evaluations (I_I). ASC was elevated in the plasma of the N_I group compared to the N_N and I_I groups. Additionally, Aβ₄₂ was increased in the plasma in the N_I and I_I groups compared to the N_N group. Importantly, the area under the curve (AUC) for ASC in participants older than 70 years old in N_N vs. N_I groups was 0.81, indicating that ASC is a promising plasma biomarker for early detection of cognitive decline. Full article

(This article belongs to the Topic Inflammaging: The Immunology of Aging)

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13 pages, 588 KiB

Open AccessSystematic Review

Immunosenescence and Inflammation in Chronic Obstructive Pulmonary Disease: A Systematic Review

by Fabíola Ramos Jesus, Fabine Correia Passos, Michelle Miranda Lopes Falcão, Marcelo Vincenzo Sarno Filho, Ingrid Lorena Neves da Silva, Anna Clara Santiago Moraes, Margarida Célia Lima Costa Neves and Gyselle Chrystina Baccan

J. Clin. Med. 2024, 13(12), 3449; https://doi.org/10.3390/jcm13123449 - 13 Jun 2024

Cited by 4 | Viewed by 1564

Abstract

Background/Objectives: Chronic Obstructive Pulmonary Disease (COPD) is a disease of premature aging, characterized by airflow limitations in the lungs and systemic chronic inflammation. This systematic review aimed to provide a systematic overview of immunosenescence and inflammation in Chronic Obstructive Pulmonary Disease (COPD). [...] Read more.

Background/Objectives: Chronic Obstructive Pulmonary Disease (COPD) is a disease of premature aging, characterized by airflow limitations in the lungs and systemic chronic inflammation. This systematic review aimed to provide a systematic overview of immunosenescence and inflammation in Chronic Obstructive Pulmonary Disease (COPD). Methods: The PubMed, Science Direct, Scopus, Cochrane Library, and Web of Science databases were searched for studies on markers of immunosenescence. Observational studies comparing patients with COPD to individuals without disease were evaluated, considering the following markers: inflammation and senescence in COPD, naïve, memory, and CD28^null T cells, and telomere length in leukocytes. Results: A total of 15 studies were included, eight of which were rated as high quality. IL-6 production, telomere shortening, and the higher frequencies of CD28^null T cells were more prominent findings in the COPD studies analyzed. Despite lung function severity being commonly investigated in the included studies, the importance of this clinical marker to immunosenescence remains inconclusive. Conclusions: The findings of this systematic review confirmed the presence of accelerated immunosenescence, in addition to systemic inflammation, in stable COPD patients. Further studies are necessary to more comprehensively evaluate the impact of immunosenescence on lung function in COPD. Full article

(This article belongs to the Topic Inflammaging: The Immunology of Aging)

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19 pages, 3823 KiB

Open AccessArticle

Mitochondrial Oxidative Stress Regulates FOXP3+ T-Cell Activity and CD4-Mediated Inflammation in Older Adults with Frailty

by Jappreet Singh Gill, Benu Bansal, Kai Guo, Fang Huang, Harpreet Singh, Junguk Hur, Nadeem Khan and Ramkumar Mathur

Int. J. Mol. Sci. 2024, 25(11), 6235; https://doi.org/10.3390/ijms25116235 - 5 Jun 2024

Cited by 4 | Viewed by 2699

Abstract

In healthy older adults, the immune system generally preserves its response and contributes to a long, healthy lifespan. However, rapid deterioration in immune regulation can lead to chronic inflammation, termed inflammaging, which accelerates pathological aging and diminishes the quality of life in older [...] Read more.

In healthy older adults, the immune system generally preserves its response and contributes to a long, healthy lifespan. However, rapid deterioration in immune regulation can lead to chronic inflammation, termed inflammaging, which accelerates pathological aging and diminishes the quality of life in older adults with frailty. A significant limitation in current aging research is the predominant focus on comparisons between young and older populations, often overlooking the differences between healthy older adults and those experiencing pathological aging. Our study elucidates the intricate immunological dynamics of the CD4/Treg axis in frail older adults compared to comparable age-matched healthy older adults. By utilizing publicly available RNA sequencing and single-cell RNA sequencing (scRNAseq) data from peripheral blood mononuclear cells (PBMCs), we identified a specific Treg cell subset and transcriptional landscape contributing to the dysregulation of CD4⁺ T-cell responses. We explored the molecular mechanisms underpinning Treg dysfunction, revealing that Tregs from frail older adults exhibit reduced mitochondrial protein levels, impairing mitochondrial oxidative phosphorylation. This impairment is driven by the TNF/NF-kappa B pathway, leading to cumulative inflammation. Further, we gained a deeper understanding of the CD4/Treg axis by predicting the effects of gene perturbations on cellular signaling networks. Collectively, these findings highlight the age-related relationship between mitochondrial dysfunction in the CD4/Treg axis and its role in accelerating aging and frailty in older adults. Targeting Treg dysfunction offers a critical basis for developing tailored therapeutic strategies aimed at improving the quality of life in older adults. Full article

(This article belongs to the Topic Inflammaging: The Immunology of Aging)

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17 pages, 3238 KiB

Open AccessArticle

Inhibition of Amyloid-β (Aβ)-Induced Cognitive Impairment and Neuroinflammation in CHI3L1 Knockout Mice through Downregulation of ERK-PTX3 Pathway

by Hyeon Joo Ham, Yong Sun Lee, Ja Keun Koo, Jaesuk Yun, Dong Ju Son, Sang-Bae Han and Jin Tae Hong

Int. J. Mol. Sci. 2024, 25(10), 5550; https://doi.org/10.3390/ijms25105550 - 19 May 2024

Cited by 7 | Viewed by 2223

Abstract

Several clinical studies reported that the elevated expression of Chitinase-3-like 1 (CHI3L1) was observed in patients suffering from a wide range of diseases: cancer, metabolic, and neurological diseases. However, the role of CHI3L1 in AD is still unclear. Our previous study demonstrated that [...] Read more.

Several clinical studies reported that the elevated expression of Chitinase-3-like 1 (CHI3L1) was observed in patients suffering from a wide range of diseases: cancer, metabolic, and neurological diseases. However, the role of CHI3L1 in AD is still unclear. Our previous study demonstrated that 2-({3-[2-(1-Cyclohexen-1-yl)ethyl]-6,7-dimethoxy-4-oxo-3,4-dihydro-2-quinazolinyl}culfanyl)-N-(4-ethylphenyl)butanamide, a CHI3L1 inhibiting compound, alleviates memory and cognitive impairment and inhibits neuroinflammation in AD mouse models. In this study, we studied the detailed correlation of CHI3L1 and AD using serum from AD patients and using CHI3L1 knockout (KO) mice with Aβ infusion (300 pmol/day, 14 days). Serum levels of CHI3L1 were significantly elevated in patients with AD compared to normal subjects, and receiver operating characteristic (ROC) analysis data based on serum analysis suggested that CHI3L1 could be a significant diagnostic reference for AD. To reveal the role of CHI3L1 in AD, we investigated the CHI3L1 deficiency effect on memory impairment in Aβ-infused mice and microglial BV-2 cells. In CHI3L1 KO mice, Aβ infusion resulted in lower levels of memory dysfunction and neuroinflammation compared to that of WT mice. CHI3L1 deficiency selectively inhibited phosphorylation of ERK and IκB as well as inhibition of neuroinflammation-related factors in vivo and in vitro. On the other hand, treatment with recombinant CHI3L1 increased neuroinflammation-related factors and promoted phosphorylation of IκB except for ERK in vitro. Web-based gene network analysis and our results showed that CHI3L1 is closely correlated with PTX3. Moreover, in AD patients, we found that serum levels of PTX3 were correlated with serum levels of CHI3L1 by Spearman correlation analysis. These results suggest that CHI3L1 deficiency could inhibit AD development by blocking the ERK-dependent PTX3 pathway. Full article

(This article belongs to the Topic Inflammaging: The Immunology of Aging)

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10 pages, 978 KiB

Open AccessBrief Report

Changes in Interleukin-1β, Tumor Necrosis Factor-α, and Interleukin-10 Cytokines in Older People with Periodontitis

by Ines Augustina Sumbayak, Sri Lelyati C. Masulili, Fatimah Maria Tadjoedin, Benso Sulijaya, Arrum Mutiara, Diana Khoirowati, Yuniarti Soeroso and Boy M. Bachtiar

Geriatrics 2023, 8(4), 79; https://doi.org/10.3390/geriatrics8040079 - 10 Aug 2023

Cited by 9 | Viewed by 2508

Abstract

Aging can change the ability to respond to various stimuli and physical conditions. A decreased immune response is a form of deterioration of function in older people, who then become more vulnerable when exposed to pathogens. Periodontitis is an inflammatory disease of the [...] Read more.

Aging can change the ability to respond to various stimuli and physical conditions. A decreased immune response is a form of deterioration of function in older people, who then become more vulnerable when exposed to pathogens. Periodontitis is an inflammatory disease of the periodontal tissues that often occurs in older people. This study aimed to clinically analyze the periodontal status and cytokine levels of IL-1β, TNF-α, and IL-10 in older people and adults with periodontitis. This clinical study examined 20 persons in a group of older people and 20 persons in a group of adults. The clinical measurements of periodontal status included the Simplified Oral Hygiene Index (OHI-S), Plaque Index (PlI), and Papilla Bleeding Index (PBI). The cytokine levels in gingival crevicular fluid (GCF) were quantified by using ELISA kits. The OHI-S, PlI, and PBI were found to be higher in the older group. The mean values of cytokines were higher in the older group than in adults, although no statistically significant differences were found. A strong correlation was found between the clinical measurements and the cytokine levels in the GCF. There was an increasing tendency of pro-inflammatory and anti-inflammatory cytokines in the older group compared to the adult group. Full article

(This article belongs to the Topic Inflammaging: The Immunology of Aging)

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13 pages, 1866 KiB

Open AccessArticle

Sex Differences in the Inflammatory Profile in the Brain of Young and Aged Mice

by Brianna Cyr and Juan Pablo de Rivero Vaccari

Cells 2023, 12(10), 1372; https://doi.org/10.3390/cells12101372 - 12 May 2023

Cited by 14 | Viewed by 2912

Abstract

Neurodegenerative diseases are a leading cause of death worldwide with no cures identified. Thus, there is a critical need for preventative measures and treatments as the number of patients is expected to increase. Many neurodegenerative diseases have sex-biased prevalence, indicating a need to [...] Read more.

Neurodegenerative diseases are a leading cause of death worldwide with no cures identified. Thus, there is a critical need for preventative measures and treatments as the number of patients is expected to increase. Many neurodegenerative diseases have sex-biased prevalence, indicating a need to examine sex differences when investigating prevention and treatment strategies. Inflammation is a key contributor to many neurodegenerative diseases and is a promising target for prevention since inflammation increases with age, which is known as inflammaging. Here, we analyzed the protein expression levels of cytokines, chemokines, and inflammasome signaling proteins in the cortex of young and aged male and female mice. Our results show an increase in caspase-1, interleukin (IL)-1β, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and ASC specks in females compared to males. Additionally, there was an increase in IL-1α, VEGF-A, CCL3, CXCL1, CCL4, CCL17, and CCL22 in aging females and an increase in IL-8, IL-17a, IL-7, LT-α, and CCL22 in aging males. IL-12/IL-23p40, CCL13, and IL-10 were increased in females compared to males but not with age. These results indicate that there are sex differences in cortical inflammaging and provide potential targets to attenuate inflammation to prevent the development of neurodegenerative disease. Full article

(This article belongs to the Topic Inflammaging: The Immunology of Aging)

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18 pages, 1189 KiB

Open AccessReview

Alzheimer’s Disease: From Immune Homeostasis to Neuroinflammatory Condition

by Lucia Princiotta Cariddi, Marco Mauri, Marco Cosentino, Maurizio Versino and Franca Marino

Int. J. Mol. Sci. 2022, 23(21), 13008; https://doi.org/10.3390/ijms232113008 - 27 Oct 2022

Cited by 22 | Viewed by 4267

Abstract

Alzheimer’s Disease is the most common cause in the world of progressive cognitive decline. Although many modifiable and non-modifiable risk factors have been proposed, in recent years, neuroinflammation has been hypothesized to be an important contributing factor of Alzheimer’s Disease pathogenesis. Neuroinflammation can [...] Read more.

Alzheimer’s Disease is the most common cause in the world of progressive cognitive decline. Although many modifiable and non-modifiable risk factors have been proposed, in recent years, neuroinflammation has been hypothesized to be an important contributing factor of Alzheimer’s Disease pathogenesis. Neuroinflammation can occur through the combined action of the Central Nervous System resident immune cells and adaptive peripheral immune system. In the past years, immunotherapies for neurodegenerative diseases have focused wrongly on targeting protein aggregates Aβ plaques and NFT treatment. The role of both innate and adaptive immune cells has not been fully clarified, but several data suggest that immune system dysregulation plays a key role in neuroinflammation. Recent studies have focused especially on the role of the adaptive immune system and have shown that inflammatory markers are characterized by increased CD4+ Teff cells’ activities and reduced circulating CD4+ Treg cells. In this review, we discuss the key role of both innate and adaptive immune systems in the degeneration and regeneration mechanisms in the pathogenesis of Alzheimer’s Disease, with a focus on how the crosstalk between these two systems is able to sustain brain homeostasis or shift it to a neurodegenerative condition. Full article

(This article belongs to the Topic Inflammaging: The Immunology of Aging)

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14 pages, 3499 KiB

Open AccessArticle

AMPK Amplifies IL2–STAT5 Signaling to Maintain Stability of Regulatory T Cells in Aged Mice

by Ram Hari Pokhrel, Ben Kang, Maheshwor Timilshina and Jae-Hoon Chang

Int. J. Mol. Sci. 2022, 23(20), 12384; https://doi.org/10.3390/ijms232012384 - 16 Oct 2022

Cited by 10 | Viewed by 3040

Abstract

AMP-activated protein kinase (AMPK), an important regulator of the aging process, is expressed in various immune cells. However, its role in regulatory T cell (Treg) stability during aging is poorly understood. Here, we addressed the role of AMPK in Treg function and stability [...] Read more.

AMP-activated protein kinase (AMPK), an important regulator of the aging process, is expressed in various immune cells. However, its role in regulatory T cell (Treg) stability during aging is poorly understood. Here, we addressed the role of AMPK in Treg function and stability during aging by generating Treg-specific AMPKα1 knockout mice. In this study, we found that AMPKα1-deficient Tregs failed to control inflammation as effectively as normal Tregs did during aging. AMPK knockout from Tregs reduces STAT5 phosphorylation in response to interleukin (IL)-2 stimulation, thereby destabilizing Tregs by decreasing CD25 expression. Thus, our study addressed the role of AMPK in Tregs in sensing IL-2 signaling to amplify STAT5 phosphorylation, which, in turn, supports Treg stability by maintaining CD25 expression and controlling inflamm-aging. Full article

(This article belongs to the Topic Inflammaging: The Immunology of Aging)

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10 pages, 1718 KiB

Open AccessArticle

Senescence-Independent Anti-Inflammatory Activity of the Senolytic Drugs Dasatinib, Navitoclax, and Venetoclax in Zebrafish Models of Chronic Inflammation

by David Hernández-Silva, Joaquín Cantón-Sandoval, Francisco Juan Martínez-Navarro, Horacio Pérez-Sánchez, Sofia de Oliveira, Victoriano Mulero, Francisca Alcaraz-Pérez and María Luisa Cayuela

Int. J. Mol. Sci. 2022, 23(18), 10468; https://doi.org/10.3390/ijms231810468 - 9 Sep 2022

Cited by 11 | Viewed by 4798

Abstract

Telomere shortening is the main molecular mechanism of aging, but not the only one. The adaptive immune system also ages, and older organisms tend to develop a chronic pro-inflammatory status with low-grade inflammation characterized by chronic activation of the innate immune system, called [...] Read more.

Telomere shortening is the main molecular mechanism of aging, but not the only one. The adaptive immune system also ages, and older organisms tend to develop a chronic pro-inflammatory status with low-grade inflammation characterized by chronic activation of the innate immune system, called inflammaging. One of the main stimuli that fuels inflammaging is a high nutrient intake, triggering a metabolic inflammation process called metainflammation. In this study, we report the anti-inflammatory activity of several senolytic drugs in the context of chronic inflammation, by using two different zebrafish models: (i) a chronic skin inflammation model with a hypomorphic mutation in spint1a, the gene encoding the serine protease inhibitor, kunitz-type, 1a (also known as hai1a) and (ii) a non-alcoholic fatty liver disease/non-alcoholic steatohepatitis (NAFLD/NASH) model with inflammation induced by a high-fat diet. Our results show that, although these models do not manifest premature aging, the senolytic drugs dasatinib, navitoclax, and venetoclax have an anti-inflammatory effect that results in the amelioration of chronic inflammation. Full article

(This article belongs to the Topic Inflammaging: The Immunology of Aging)

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12 pages, 1987 KiB

Open AccessArticle

Dual-Energy Computed Tomography-Based Quantitative Bone Marrow Imaging in Non-Hematooncological Subjects: Associations with Age, Gender and Other Variables

by Florian Hagen, Jan Fritz, Antonia Mair, Marius Horger and Malte N. Bongers

J. Clin. Med. 2022, 11(14), 4094; https://doi.org/10.3390/jcm11144094 - 14 Jul 2022

Cited by 3 | Viewed by 2574

Abstract

Background: Our aim is to assess the utility and associations of quantitative bone marrow attenuation (BMA) values measured on clinical dual-energy computed tomography (DECT) exams in non-hematooncologic subjects with skeletal regions, patient age, gender, and other clinical variables. Methods: Our local ethics committee [...] Read more.

Background: Our aim is to assess the utility and associations of quantitative bone marrow attenuation (BMA) values measured on clinical dual-energy computed tomography (DECT) exams in non-hematooncologic subjects with skeletal regions, patient age, gender, and other clinical variables. Methods: Our local ethics committee approved this retrospective image data analysis. Between July 2019 and July 2021, 332 eligible patients (mean age, 64 ± 18 years; female, 135) were identified. Inclusion criteria were the availability of a standardized abdominopelvic DECT data set acquired on the same scanner with identical protocol. Eleven regions-of-interest were placed in the T11-L5 vertebral bodies, dorsal iliac crests, and femur necks. Patient age, gender, weight, clinical, habitual variables, inflammation markers, and anemia were documented in all cases. Results: Multi-regression analyses (all, p < 0.05) identified age as the strongest predictor of lumbar BMA (standardized coefficient: β = −0.74), followed by CRP (β = 0.11), LDH (β = 0.11), and gender (β = −0.10). In the lower thoracic spine, age was the strongest predictor (β = −0.58) of BMA, followed by gender (β = −0.09) and LDH (β = 0.12). In femoral bones, age was negatively predictive of BMA (β = −0.12), whereas LDH and anemia were positively predictive (β = 0.16 both). Heart insufficiency significantly decreased (β = 0.12, p = 0.034) a BMA value gradient from higher to lower HU values along the vertebrae T11 and L5, whereas age significantly increased this gradient (β = −0.2, p ≤ 0.001). Conclusions: DECT-based BMA measurements can be obtained from clinical CT exams. BMA values are negatively associated with patient age and influenced by gender, anemia, and inflammatory markers. Full article

(This article belongs to the Topic Inflammaging: The Immunology of Aging)

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17 pages, 5757 KiB

Open AccessArticle

Mesenchymal Stem Cells and Extracellular Vesicles Derived from Canine Adipose Tissue Ameliorates Inflammation, Skin Barrier Function and Pruritus by Reducing JAK/STAT Signaling in Atopic Dermatitis

by Sung Youl Kim, Tae Hong Yoon, Jungtae Na, Seong Joon Yi, Yunseok Jin, Minji Kim, Tae-Ho Oh and Tae-Wook Chung

Int. J. Mol. Sci. 2022, 23(9), 4868; https://doi.org/10.3390/ijms23094868 - 27 Apr 2022

Cited by 19 | Viewed by 4675

Abstract

Canine atopic dermatitis (AD) is a common chronic inflammatory skin disorder resulting from imbalance between T lymphocytes. Current canine AD treatments use immunomodulatory drugs, but some of the dogs have limitations that do not respond to standard treatment, or relapse after a period [...] Read more.

Canine atopic dermatitis (AD) is a common chronic inflammatory skin disorder resulting from imbalance between T lymphocytes. Current canine AD treatments use immunomodulatory drugs, but some of the dogs have limitations that do not respond to standard treatment, or relapse after a period of time. Thus, the purpose of this study was to evaluate the immunomodulatory effect of mesenchymal stem cells derived from canine adipose tissue (cASCs) and cASCs-derived extracellular vesicles (cASC-EVs) on AD. First, we isolated and characterized cASCs and cASCs-EVs to use for the improvement of canine atopic dermatitis. Here, we investigated the effect of cASCs or cASC-EVs on DNCB-induced AD in mice, before using for canine AD. Interestingly, we found that cASCs and cASC-EVs improved AD-like dermatitis, and markedly decreased levels of serum IgE, (49.6%, p = 0.002 and 32.1%, p = 0.016 respectively) epidermal inflammatory cytokines and chemokines, such as IL-4 (32%, p = 0.197 and 44%, p = 0.094 respectively), IL-13 (47.4%, p = 0.163, and 50.0%, p = 0.039 respectively), IL-31 (64.3%, p = 0.030 and 76.2%, p = 0.016 respectively), RANTES (66.7%, p = 0.002 and 55.6%, p = 0.007) and TARC (64%, p = 0.016 and 86%, p = 0.010 respectively). In addition, cASCs or cASC-EVs promoted skin barrier repair by restoring transepidermal water loss, enhancing stratum corneum hydration and upregulating the expression levels of epidermal differentiation proteins. Moreover, cASCs or cASC-EVs reduced IL-31/TRPA1-mediated pruritus and activation of JAK/STAT signaling pathway. Taken together, these results suggest the potential of cASCs or cASC-EVs for the treatment of chronic inflammation and damaged skin barrier in AD or canine AD. Full article

(This article belongs to the Topic Inflammaging: The Immunology of Aging)

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17 pages, 1341 KiB

Open AccessReview

Senescence-Associated Cell Transition and Interaction (SACTAI): A Proposed Mechanism for Tissue Aging, Repair, and Degeneration

by Yajun Liu, Jonah Schwam and Qian Chen

Cells 2022, 11(7), 1089; https://doi.org/10.3390/cells11071089 - 24 Mar 2022

Cited by 11 | Viewed by 5171

Abstract

Aging is a broad process that occurs as a time-dependent functional decline and tissue degeneration in living organisms. On a smaller scale, aging also exists within organs, tissues, and cells. As the smallest functional unit in living organisms, cells “age” by reaching senescence [...] Read more.

Aging is a broad process that occurs as a time-dependent functional decline and tissue degeneration in living organisms. On a smaller scale, aging also exists within organs, tissues, and cells. As the smallest functional unit in living organisms, cells “age” by reaching senescence where proliferation stops. Such cellular senescence is achieved through replicative stress, telomere erosion and stem cell exhaustion. It has been shown that cellular senescence is key to tissue degradation and cell death in aging-related diseases (ARD). However, senescent cells constitute only a small percentage of total cells in the body, and they are resistant to death during aging. This suggests that ARD may involve interaction of senescent cells with non-senescent cells, resulting in senescence-triggered death of non-senescent somatic cells and tissue degeneration in aging organs. Here, based on recent research evidence from our laboratory and others, we propose a mechanism—Senescence-Associated Cell Transition and Interaction (SACTAI)—to explain how cell heterogeneity arises during aging and how the interaction between somatic cells and senescent cells, some of which are derived from aging somatic cells, results in cell death and tissue degeneration. Full article

(This article belongs to the Topic Inflammaging: The Immunology of Aging)

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15 pages, 531 KiB

Open AccessReview

Cardiovascular Inflammaging: Mechanisms and Translational Aspects

by Maria Luisa Barcena, Muhammad Aslam, Sofya Pozdniakova, Kristina Norman and Yury Ladilov

Cells 2022, 11(6), 1010; https://doi.org/10.3390/cells11061010 - 16 Mar 2022

Cited by 39 | Viewed by 7026

Abstract

Aging is one of the major non-reversible risk factors for several chronic diseases, including cancer, type 2 diabetes, dementia, and cardiovascular diseases (CVD), and it is a key cause of multimorbidity, disability, and frailty (decreased physical activity, fatigue, and weight loss). The underlying [...] Read more.

Aging is one of the major non-reversible risk factors for several chronic diseases, including cancer, type 2 diabetes, dementia, and cardiovascular diseases (CVD), and it is a key cause of multimorbidity, disability, and frailty (decreased physical activity, fatigue, and weight loss). The underlying cellular mechanisms are complex and consist of multifactorial processes, such as telomere shortening, chronic low-grade inflammation, oxidative stress, mitochondrial dysfunction, accumulation of senescent cells, and reduced autophagy. In this review, we focused on the molecular mechanisms and translational aspects of cardiovascular aging-related inflammation, i.e., inflammaging. Full article

(This article belongs to the Topic Inflammaging: The Immunology of Aging)

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