Dietary restriction (DR) slows aging in many animals, while in some cases, the sensory signals from diet alone are sufficient to retard or accelerate lifespan. The digestive tract is a candidate location to sense nutrients, where neuropeptides secreted by enteroendocrine cells (EEC) produce systemic signals in response to food. Here, we measure how Drosophila neuropeptide F (NPF) is secreted into adult circulation by EEC and find that specific EEC differentially respond to dietary sugar and yeast. Female lifespan is increased when gut NPF is genetically depleted, and this manipulation is sufficient to blunt the longevity benefit conferred by DR. Depletion of NPF receptors at insulin-producing neurons of the brain also increases female lifespan, consistent with observations where loss of gut NPF decreases neuronal insulin secretion. The longevity conferred by repressing gut NPF and brain NPF receptors is reversed by treating adults with a juvenile hormone (JH) analog. JH is produced by the adult corpora allata, and inhibition of the insulin receptor at this tissue decreases JH titer and extends lifespan in both males and females, while this longevity is restored to wild type by treating adults with a JH analog. Overall, EEC of the gut modulate Drosophila aging through interorgan communication mediated by a gut-brain-corpora allata axis, and insulin produced in the brain impacts lifespan through its control of JH titer. These data suggest that we consider how human incretins and their analogs, which are used to treat obesity and diabetes, may impact aging.

• Klíčová slova
• aging, incretin, insulin, interorgan communication, juvenile hormone,
• MeSH
• dlouhověkost fyziologie   MeSH
• Drosophila melanogaster metabolismus   MeSH
• enteroendokrinní buňky metabolismus   MeSH
• inzulin * metabolismus   MeSH
• juvenilní hormony * metabolismus   MeSH
• mozek metabolismus   MeSH
• neurony metabolismus   MeSH
• neuropeptidy * metabolismus   MeSH
• osa mozek-střevo * fyziologie   MeSH
• proteiny Drosophily * metabolismus   genetika   MeSH
• stárnutí metabolismus   fyziologie   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• inzulin * MeSH
• juvenilní hormony * MeSH
• neuropeptide F, Drosophila MeSH Prohlížeč
• neuropeptidy * MeSH
• proteiny Drosophily * MeSH

The biosynthesis of ribosomes is a complex process that requires the coordinated action of many factors and a huge energy investment from the cell. Ribosomes are essential for protein production, and thus for cellular survival, growth and proliferation. Ribosome biogenesis is initiated in the nucleolus and includes: the synthesis and processing of ribosomal RNAs, assembly of ribosomal proteins, transport to the cytoplasm and association of ribosomal subunits. The disruption of ribosome biogenesis at various steps, with either increased or decreased expression of different ribosomal components, can promote cell cycle arrest, senescence or apoptosis. Additionally, interference with ribosomal biogenesis is often associated with cancer, aging and age-related degenerative diseases. Here, we review current knowledge on impaired ribosome biogenesis, discuss the main factors involved in stress responses under such circumstances and focus on examples with clinical relevance.

• Klíčová slova
• aging, cancer, p53, ribosome biogenesis, ribosomopathy,
• MeSH
• biogeneze organel MeSH
• lidé MeSH
• nádory metabolismus   MeSH
• ribozomální proteiny metabolismus   MeSH
• ribozomy metabolismus   MeSH
• stárnutí metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• ribozomální proteiny MeSH

• Klíčová slova
• aging, cancer, cell differentiation, mitochondria, retrograde signaling, yeast colonies,
• MeSH
• buněčná diferenciace fyziologie   MeSH
• lidé MeSH
• mitochondrie metabolismus   MeSH
• signální transdukce fyziologie   MeSH
• stárnutí buněk fyziologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• úvodníky MeSH

Aging is an extremely complex phenomenon that has many manifestations at the molecular, cellular, and whole-body levels, and in some form involves virtually all living beings. It is a process characterized by a general progressive deterioration of the physiological functions of the organism leading to increased susceptibility to diseases. This article summarizes the basic features and molecular hallmarks of aging and describes some of the genetic mechanisms of this phenomenon. It deals with the particular genes and molecular pathways involved in the regulation of aging as well as promising possibilities of interventions affecting this process.

• Klíčová slova
• aging, genetics, longevity genes, sirtuins, telomeres,
• MeSH
• dlouhověkost * MeSH
• lidé MeSH
• stárnutí * genetika   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH

• Klíčová slova
• AGING/physiology *,
• MeSH
• lidé MeSH
• stárnutí fyziologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH

• Klíčová slova
• Alzheimer’s disease, aging, basal forebrain, hippocampus, spatial navigation,
• MeSH
• Alzheimerova nemoc patologie   MeSH
• hipokampus patologie   fyziologie   MeSH
• kognitivní dysfunkce patologie   MeSH
• lidé MeSH
• prostorová navigace * MeSH
• stárnutí * MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• práce podpořená grantem MeSH
• úvodníky MeSH

Aging is a natural, gradual, and inevitable process associated with a series of changes at the molecular, cellular, and tissue levels that can lead to an increased risk of many diseases, including cancer. The most significant changes at the genomic level (DNA damage, telomere shortening, epigenetic changes) and non-genomic changes are referred to as hallmarks of aging. The hallmarks of aging and cancer are intertwined. Many studies have focused on genomic hallmarks, but non-genomic hallmarks are also important and may additionally cause genomic damage and increase the expression of genomic hallmarks. Understanding the non-genomic hallmarks of aging and cancer, and how they are intertwined, may lead to the development of approaches that could influence these hallmarks and thus function not only to slow aging but also to prevent cancer. In this review, we focus on non-genomic changes. We discuss cell senescence, disruption of proteostasis, deregualation of nutrient sensing, dysregulation of immune system function, intercellular communication, mitochondrial dysfunction, stem cell exhaustion and dysbiosis.

• Klíčová slova
• aging, cancer, hallmarks, non-genomic,
• MeSH
• lidé MeSH
• mezibuněčná komunikace MeSH
• nádory * MeSH
• stárnutí buněk genetika   MeSH
• stárnutí * metabolismus   MeSH
• zkracování telomer MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

This article examines the hypothesis that the dialogical integration of life experiences is related to successful aging. Life story interviews with 93 older Czech adults were sorted into categories characterized by specific patterns of life experience integration: (i) without dialogical processes, (ii) with differentiated I-positions, (iii) with dialogical relationships, (iv) partially integrated, and (v) completely integrated. The results indicated that the categories were ordered, yielding low-level correlations with scales of successful aging in predicted directions. A comparison of the categories revealed that they were related to successful aging in a cumulative way, starting with the most essential indicator (lower scores of rumination) in the participants who had developed at least dialogical relationships, continuing to higher well-being linked with partial integration, and ending with an advanced indicator (optimism toward future) linked with complete integration. These relationships were summarized in a hypothetical model that is open to further examination.

• Klíčová slova
• dialogical self, future time perspective, life review, life story interview, meaning making, narrative analysis, older adults, reminiscence, successful aging, well-being,
• MeSH
• kognitivní ruminace MeSH
• lidé MeSH
• optimismus psychologie   MeSH
• rozhovory jako téma MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• vyprávění * MeSH
• zdravé stárnutí * psychologie   MeSH
• zdravotní stav MeSH
• životní změny * MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• senioři nad 80 let MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Geografické názvy
• Česká republika MeSH

Ageing is associated with the accumulation of damage to all the macromolecules within and outside cells leading to progressively more cellular and tissue defects and resulting in age-related frailty, disability and disease. As a result of the aging process the bone deteriorates in composition, structure and function. Age-related musculoskeletal losses are a major public health burden because they can cause physical disability and increased mortality. We tried to find out on a small set of old women, without risk factors for osteoporosis, what caused them the loss of bone minerals. All 492 women had just only one risk factor - the old age. Laboratory findings have shown a decreased serum C telopeptide and low serum alkaline phosphatase circulating markers, used to quantify bone resorption and formation, and very low level of vitamin D. Very low level of vitamin D that disrupted calcium absorption through the intestine, and decreased calcemia increased parathyroid hormone levels with resulting bone effect. The manifestation of physiological aging is worsening eyesight, peripheral neuropathy, depression, worsening of physical condition, skin aging, sarcopenia and bone mineral loss. Senile osteoporosis, which is not caused by known risk factors for osteoporosis, does not appear to be a separate disease, but is part of the physiological process of aging. Treatment of senile osteoporosis should be focused on the control of secondary hyperparathyroidism by administration of vitamin D and calcium. The risk of fractures in the advanced age is determined by a large number of factors ranging from hazards in the home environment to frailty and poor balance.

• Klíčová slova
• Aging, Frailty, Osteoporosis, Sarcopenia,
• MeSH
• alkalická fosfatasa krev   MeSH
• kolagen typu I krev   MeSH
• kostní denzita MeSH
• lidé MeSH
• osteogeneze MeSH
• osteoporóza krev   MeSH
• parathormon krev   MeSH
• peptidy krev   MeSH
• stárnutí krev   patologie   MeSH
• vápník metabolismus   MeSH
• vitamin D krev   MeSH
• Check Tag
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• alkalická fosfatasa MeSH
• collagen type I trimeric cross-linked peptide MeSH Prohlížeč
• kolagen typu I MeSH
• parathormon MeSH
• peptidy MeSH
• vápník MeSH
• vitamin D MeSH

Understanding the molecular mechanism of aging could have enormous medical implications. Despite a century of research, however, there is no universally accepted theory regarding the molecular basis of aging. On the other hand, there is plentiful evidence suggesting that DNA constitutes the central molecule in this process. Here, we review the roles of chromatin structure, DNA damage, and shortening of telomeres in aging and propose a hypothesis for how their interplay leads to aging phenotypes.

• Klíčová slova
• Aging, Chromatin structure, DNA, DNA damage, DNA repair, Mutagenesis, Telomeres,
• MeSH
• chromatin ultrastruktura   MeSH
• DNA chemie   genetika   MeSH
• lidé MeSH
• oprava DNA fyziologie   MeSH
• poškození DNA fyziologie   MeSH
• stárnutí genetika   MeSH
• zkracování telomer MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• chromatin MeSH
• DNA MeSH