Perhaps the most recognizable consequences of tissue aging are manifest in the skin. Hair graying and loss, telltale wrinkles, and age spots are indicative of physiological aging symptoms, many of which are analogous to processes in other tissues as well with less visible outcomes. While the study of skin aging has been conducted for decades, more recent work has illuminated many of the fundamental

Calcium (Ca2+) homeostasis is disrupted during aging in several cell types and this disruption leads to autophagy impairment. The mechanisms regarding Ca2+, senescence, and autophagy need to be elucidated. Therefore, we hypothesized that cellular senescence can be improved by regulating Ca2+ level and autophagy activity. We identified that hydrogen peroxide (H2O2)-induced senescence was accompanied

Age is the only one non-modifiable risk of cerebral ischemia. Advances in stroke medicine and behavioral adaptation to stroke risk factors and comorbidities was successful in decreasing stroke incidence and increasing the number of stroke survivors in western societies. Comorbidities aggravates the outcome after cerebral ischemia. However, due to the increased in number of elderly, the incidence of

Fumarylacetoacetate hydrolase (FAH) superfamily members are commonly expressed in the prokaryotic kingdom, where they take part in the committing steps of degradation pathways of complex carbon sources. Besides FAH itself, the only described FAH superfamily members in the eukaryotic kingdom are fumarylacetoacetate hydrolase domain containing proteins (FAHD) 1 and 2, that have been a focus of recent

Vascular tree development depends on the timely differentiation of endothelial and vascular smooth muscle cells. These latter are key players in the formation of the vascular scaffold that offers resistance to the blood flow. This review aims at providing an overview on the role of PDE5, the cGMP-specific phosphodiesterase that historically attracted much attention for its involvement in male impotence

The recent advent of ‘organs in a dish’ has revolutionised the research landscape. These 3D culture systems have paved the way for translational, post genomics research by enabling scientists to model diseases in the laboratory, grow patient-derived organoids, and unite this technology with other cutting-edge methodologies such as drug discovery. Fields such as dermatology and neuroscience have revolutionised

The interrogation of established, large-scale datasets presents great opportunities in health data science for the linkage and mining of potentially disparate resources to create new knowledge in a fast and cost-efficient manner. The number of datasets that can be queried in the field of multimorbidity is vast, ranging from national administrative and audit datasets, large clinical, technical and biological

So far, the investigation of stem cell aging has been primarily carried out at the genomic level to follow transcriptome changes, clonal dominance, epigenetic changes, and, more recently, population heterogeneity by single cell sequencing. Here, we review recent findings in the field of stem cell aging that include failure of proteostasis, the impact of age-related metabolic changes on stem cell differentiation

Intervertebral disc (IVD) degeneration (IDD) is identified as an abnormal, cell-mediated, age-dependent and genetics-dependent molecular degeneration process in which NPCs (nucleus pulposus cells) senesce and the balance of ECM (extracellular matrix) synthesis and catabolism is disrupted. Increasing evidence reveals that IDD can be modulated by genetic factors, including non-coding RNAs. In the present

Autophagy is a major self-degradative intracellular process required for the maintenance of homeostasis and promotion of survival in response to starvation. It plays critical roles in a large variety of physiological and pathological processes. On the other hand, aberrant regulation of autophagy can lead to various cancers and neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease

Glycosylphosphatidylinositol (GPI)-anchored proteins (GPI-APs) are associated with the surface of eucaryotic cells only through a covalently coupled carboxy-terminal GPI glycolipid structure which is anchored at the outer leaflet of plasma membranes. This mode of membrane association may be responsible for the recent observations that full-length GPI-APs harbouring the complete GPI anchor are (i) released

The glucose homeostasis is essential for brain function, and energy deficiency is a key feature of brain aging. We investigated whether improving glucose metabolism in the auditory cortex can delay the aging of auditory function of guinea pigs with age-related hearing loss (ARHL) by d-galactose. Auditory function was assessed by auditory brainstem response (ABR), glucose metabolism was detected by

Type 2 diabetes mellitus (T2DM) is a global disease that poses a significant threat to public health. The incidence of both diabetes and dementia has increased simultaneously. Researchers have found that a large proportion of dementia patients have T2DM. In recent years, increasing evidence has demonstrated a link between cognitive decline and T2DM. Although the exact pathogenesis of cognitive impairment

Senescent cells accumulate during aging in a variety of tissues. Although scarce, they could influence tissue function non-cell-autonomously via secretion of a range of factors in their neighborhood. Recent studies support a role of senescent cells in age-related morbidity, including neurodegenerative diseases, cardiovascular pathologies, cancers, aging-associated nephrological alterations, chronic

Diagnosis of Alzheimer’s disease (AD) is often difficult because of distinct and subjective clinical features, especially in the early stage. FOXO3a protein present in the cognitive centre of brain in inferior temporal region and parahippocampus. FOXO3a can be a potential novel target against AD. AD, Mild Cognitive impairment (MCI) and Geriatric Control (GC) were recruited after diagnosis by clinical

ATM is a kinase involved in DNA damage response (DDR), regulation of response to oxidative stress, autophagy and mitophagy. Mutations in the ATM gene in humans result in ataxi A–Telangiectasia disease (A–T) characterized by a variety of symptoms with neurodegeneration and premature ageing among them. Since brain is one of the most affected organs in A–T, we have focused on senescence of neural progenitor

Cell senescence – an irreversible proliferation arrest – is one of the possible cellular responses to stress. There is a vast variety of stimuli, extrinsic and intrinsic, known to induce senescence, and several molecular pathways involved in the process; yet much still remains to be explained. Senescent cells can communicate with neighboring cells through secreted factors such as cytokines and chemokines

Adenosine A2A receptors (A2AR) are crucial in facilitating the BDNF action on synaptic transmission in the rat hippocampus primarily upon ageing. Furthermore, it has been suggested that A2AR-Tropomyosin related kinase B receptor (TrkB) crosstalk has a pivotal role in adenosine A2AR-mediated modulation of the BDNF action on hippocampal plasticity. Considering the impact of the above receptors interplay

The clinical picture of multimorbidity is heterogeneous and it is characterized by great complexity. Precision medicine is an innovative approach to provide personalized care focused on individual characteristics and to deliver the right treatments, at the right time, to the right person. The precision medicine approach, which represents an epochal change in the field of chronic diseases, has been

The age-associated decline of regenerative capacity in many tissues is a consequence of stem cell intrinsic and extrinsic perturbations that are only beginning to be understood. To gain insight into mechanisms of this age-related decline, a comprehensive understanding of these perturbations is necessary. Drosophila intestinal stem cells (ISCs) have served as a prime model in which to explore these

The functional decline that is observed in HSCs upon aging is attributed mainly to cell intrinsic factors that regulate quiescence, self-renewal and differentiation. MicroRNAs (miRs) have an indispensable role in the regulation of HSCs and have been shown to also regulate processes related to tissue aging in specific cell types. Here we discuss the role of miRs in the regulation of HSC self-renewal

Extensive studies on PINK1, whose mutations are a confirmed cause of Parkinson’s disease (PD), have been conducted in animal models or immortalized cell lines. These include initial ground-breaking discoveries on mitophagy, which demonstrated that PINK1 recruits Parkin on depolarized mitochondria, initiating a signalling cascade eventually resulting in their autophagic degradation. Not all features

Aging is characterized by a progressive decline in tissue and organ function often linked to a reduced stem cell functionality, a cell population important for regeneration. Skeletal muscle mass and regenerative capacity decrease with advancing age. Muscle stem cells, also termed satellite cells, are a prerequisite for regeneration of skeletal muscle. Their functionality declines with increasing age

Ribosome biogenesis takes place mainly in the nucleolus, a nuclear, non-membrane bound organelle forming around the gene arrays encoding ribosomal RNA (rRNA). Nucleolar activity comprises synthesis, processing and maturation of rRNAs, followed by their assembly with ribosomal proteins into pre-ribosomal particles. The final formation of translation-competent ribosomes in the cytoplasm is the prerequisite

Somatic cells may be reprogrammed to pluripotent state by ectopic expression of certain transcription factors; namely, OCT4, SOX2, KLF4 and c-MYC. However, the molecular and cellular mechanisms are not adequately understood, especially for human embryonic development. Studies during the last five years implicated importance of OCT4 in human zygotic genome activation (ZGA), patterns of OCT4 protein

Clonal haematopoiesis of indeterminate potential (CHIP) is widespread in the elderly. CHIP is driven by somatic mutations in leukaemia driver genes, such as Janus Kinase 2 (JAK2), Tet methylcytosine dioxygenase 2 (TET2), ASXL Transcriptional Regulator 1 (ASXL1) and DNA (cytosine-5)-methyltransferase 3A (DNMT3A), leading to reduced diversity of the blood pool. CHIP carries an increased risk for leukaemia

Adult stem cells sustain tissue homeostasis throughout life and provide an important reservoir of cells capable of tissue repair in response to stress and tissue damage. Age-related changes to stem cells and/or the specialized niches that house them have been shown to negatively impact stem cell maintenance and activity. In addition, metabolic inputs have surfaced as another crucial layer in the control

The two transcriptional coactivators YAP/TAZ act as the downstream transducers of the Hippo pathway. Recent studies have demonstrated that those two transcriptional regulators are crucial for an organism in order to induce a regenerative response upon tissue damage. In addition, YAP/TAZ are promising targets for regenerative medicine, as artificially increasing YAP/TAZ activity can be used to stimulate

Intestinal epithelium undergoes dysfunctions and diseases over time with an exponential increase in the elderly population. Recent studies reported that the intestinal stem cells (ISCs) show a functional decline during aging and a lack of an appropriate cell identity control. Increase of cell-to-cell heterogeneity is a hallmark of aging tissues and organs, however there is little experimental evidence

The aim of the current study was to investigate the association between diet and handgrip strength. The current study included 68,002 participants (age 63.8 ± 2.7 years, 50.3% women, 49.7% men) from UK Biobank. Diet and nutritional data (carotene, retinol, potassium, vitamin C, foliate, vitamin B12, vitamin B6, iron, vitamin E, calcium, magnesium, carbohydrates, protein, polyunsaturated fat, fat, starch

Amyloid β 1–42 peptide (Aβ1–42) accumulates in Alzheimer's disease (AD) that is toxic to the basal forebrain cholinergic (BFC) neurons in substantia innominata-nucleus basalis magnocellularis complex (SI-NBM). Transient Receptor Potential Ankyrin1 (TRPA1) receptor is present in murine brain, however its role in neurotoxic processes is unclear. We investigated the Aβ1–42-induced neurotoxicity in TRPA1

Hypertension is a common age-related disease, along with vascular and neurodegenerative diseases. Vascular ageing increases during hypertension, but hypertension itself accelerates vascular ageing, thus creating a vicious circle. Vascular stiffening, endothelial dysfunction, impaired contractility and vasorelaxation are the main alterations related to vascular ageing, as a consequence of vascular smooth

Senescence is a state of proliferative arrest which has been described as a protective mechanism against the malignant transformation of cells. However, senescent cells have also been demonstrated to accumulate with age and to contribute to a variety of age-related pathologies. These pathological effects have been attributed to the acquisition of an enhanced secretory profile geared towards inflammatory

Fucoxanthin, as a main marine carotenoid, exhibit a wide variety of bioactivities, including antioxidant activity. Previously, we have shown the geroprotective activity of fucoxanthin on Drosophila and C. elegans. Our new study aimed to compare the antioxidant activity of fucoxanthin in early and late passage normal human cells LECh4(81) in physiological conditions and under oxidative stress. In addition

Mitochondria is a key cellular organelle, which is tightly supervised by multiple oversight cellular mechanisms regulating mitochondrial biogenesis and mitochondria maintenance and/or elimination. Selective autophagy of mitochondria, id est mitophagy, is one of the cellular mechanisms controlling mitochondria homeostasis. The nematode Caenorhabditis elegans has recently emerged as a powerful model

Cellular senescence is mainly characterized as a stable proliferation arrest and a senescence associated secretory phenotype (SASP). Senescence is triggered by diverse stimuli such as telomere shortening, oxidative stress, oncogene activation and DNA damage, and consequently contributes to multiple physiology and pathology outcomes, including embryonic development, wound healing and tumor suppression

Accumulation of neurotoxic forms of amyloid-β proteins in senile plaques and hyperphosphorylated tau proteins in neurofibrillary tangles is a well-known pathophysiological hallmark of Alzheimer’s disease (AD). However, clinical trials with drugs targeting amyloid-β and tau have failed to demonstrate efficacy in treating AD. All currently FDA-approved anti-AD drugs have symptomatic effects only and

Mice with an overall deletion of the sensory neuropeptide α-calcitonin gene-related peptide (α-CGRP) develop an age-dependent osteopenic bone phenotype. Underlying molecular mechanisms of how αCGRP affects bone cell metabolism are not well understood. This study aims to characterize differences in metabolic parameters of osteoblast-like cells (OB) and differentiated bone marrow-derived macrophages

Aging is a natural process that includes several changes that gradually make organisms degenerate and die. Harman's theory proposes that aging is a consequence of the progressive accumulation of oxidative modifications mediated by reactive oxygen/nitrogen species, which plays an essential role in the development and progression of many neurodegenerative diseases. This review will focus on how abnormal

Purpose This study aims to evaluate whether regular lifelong exercise has effects on age-related inflammatory cytokines, oxidative stress, and the skeletal muscle proteome. Methods Four groups of adult-aged (8-month-old) female Sprague Dawley rats were used: rats for which training was initiated at either 8 (8 M–MICT, moderate-intensity continuous training) or 18 months (18 M–MICT) and sedentary rats

INTRODUCTION Multifactorial biological processes underpin dysregulation over several individual physiological systems. However, it is challenging to characterize and model this multisystemic dysregulation and its relationship with individual physiologic systems. We operationalized a theory-driven measure of multisystem dysregulation and empirically tested for measurement differences by key characteristics

Biomarkers of aging are urgently needed to identify individuals at high risk of developing age-associated disease or disability. Growing evidence from population-based studies points to whole-body magnetic resonance imaging’s (MRI) enormous potential for quantifying subclinical disease burden and for assessing changes that occur with aging in all organ systems. The Aging Imageomics Study aims to identify

Sestrins (Sesns) represent a highly conserved family of stress-inducing proteins that are involved in antioxidant and autophagy regulatory functions. They are very important mediators as they can protect the cells under a variety of noxious stimulating conditions. However, the functions of Sesns in aging has not yet been fully understood. Here, we summarize the roles of Sesns in the aging process.

Senescence is a cellular response to stress for both dividing and post-mitotic cells. Noteworthy, long-lived post-mitotic cells (collectively named LLPMCs), which can live for decades in the organism, can exhibit a distinct type of cellular aging characterized by a progressive functional decline not associated to an overt senescence phenotype. The age-related drivers of senescence and aging in LLPMCs

Human chronotype, the temporal pattern of daily behaviors, is influenced by postnatal seasonal programming and ageing. The aim of this study was to investigate genetic variants that are associated with season of birth programming and longitudinal chronotype change. Longitudinal sleep timing and genotype data from 1449 participants were collected for up to 27 years. Gene-environment interaction analysis

While elderly patients are at high risk of fatality, research concerning COVID-19 has largely been done on clarifying the clinical features. As such, the present work aims to identify risk factors for mortality in elderly patients with COVID-19. Given that single-centre studies are less likely informative as elderly remains a minority in the total Chinese population, the present study reviewed the

Stem cell aging contributes to aging-associated tissue degeneration and dysfunction. Recent studies reveal a mitochondrial metabolic checkpoint that regulates stem cell quiescence and maintenance, and dysregulation of the checkpoint leads to functional deterioration of aged stem cells. Here, we present the evidence supporting the mitochondrial metabolic checkpoint regulating stem cell aging and demonstrating

Aging is known to affect adversely the corticosterone status and the brain function including cognition. Calorie restricted (CR) diet has been found to improve brain aging. The objective of the present investigation is to study the effect of short-term CR diet without any food deprivation on aging-induced impairment of cognitive function in relation to the corticosterone status and the brain regional

The number of elderly persons is rising rapidly, and healthspan is a key factor in determining the well-being of individuals and the sustainability of national health systems. Environmental health is crucial for a "successful aging". Complex relationships between environmental factors and non-communicable diseases play a major role, causing or accelerating disabilities. Besides genetic factors, aging

Aging is characterized by the deterioration of different cellular and organismal structures and functions. A typical hallmark of the aging process is the accumulation of dysfunctional mitochondria and excess iron, leading to a vicious cycle that promotes cell and tissue damage, which ultimately contribute to organismal aging. Accordingly, altered mitochondrial quality control pathways such as mitochondrial

Ageing and obesity have common hallmarks: altered glucose and lipid metabolism, chronic inflammation and oxidative stress are some examples. The downstream effects of SIRT1 activity have been thoroughly explored, and their research is still in expanse. SIRT1 activation has been shown to regulate pathways with beneficiary effects on 1) ageing and obesity-associated metabolic disorders such as metabolic

Aging is characterized by the functional and regenerative decline of tissues and organs. This regenerative decline is a consequence of the numerical and functional loss of adult stem cells, which are the corner stone of tissue homeostasis and repair. A palpable example of this decline is provided by skeletal muscle, a specialized tissue composed of postmitotic myofibers that contract to generate force

Fibrosis is widely observed in multiple organs, which is generally associated with aging-related diseases, including liver fibrosis, lung fibrosis, cardiac fibrosis and renal fibrosis. The excess deposition of extracellular matrix ultimately leads to the disruption of organ architecture and loss of function. H19 is paternally imprinted maternally expressed lncRNA, which is highly expressed during the

Mitochondria are essential organelles that generate energy to fuel myocardial contraction. Accumulating evidence also suggests that, in the heart, mitochondria may contribute to specific aspects of disease progression through the regulations of specific metabolic intermediates, as well as the transcriptional and epigenetic states of cells. If damaged, the mitochondria and their related pathways are

Caloric reduction (CR) is considered as the most reasonable intervention to delay aging and age-related diseases. Numerous studies in various model organisms provide the main basis for this hypothesis. Human studies exist, but they differ widely in study design, characteristics of test persons and study outcome. In this study we investigated CR in humans on a molecular level to gain a better understanding

Oncogene-induced senescence (OIS) is a powerful intrinsic tumor-suppressive mechanism, arresting cell cycle progression upon oncogene-activating genomic alterations. The discovery and characterization of the senescence-associated secretome unveiled a rich additional complexity to the senescence phenotype, including extrinsic impacts on the microenvironment and engagement of the immune response. Emerging