Inflammaging refers to the low level, chronic persistent and systemic inflammation of the body during aging without obvious infection, which is related to the chronic proinflammatory process of many aging-related diseases, and is a significant risk factor determining the incidence rate and mortality. The possible factors of inflammaging include cell senescence, mitochondrial dysfunction, and immune aging and so on. Cell senescence refers to the process of cell entering permanent cell cycle arrest. Aging cells have the characteristics of secreting senescence associated secretory phenotype (SASP) factors, including many proinflammatory factors, chemokines, growth factors and matrix degradation molecules, leading to changes of tissue microenvironment and cell biological function. Mitochondria dysfunction is a potential driver of inflammaging. With the gradual increase of mitochondria with dysfunction in the aging process, the autophagic clearance of mitochondria decreases, causing the increase of reactive oxygen species in mitochondria and the increase of dangerous associated molecular patterns from mitochondria, leading to the secretory phenotype of mitochondrial dysfunction associated senescence (MiDAS). Immune aging also plays a causal role in promoting inflammaging, leading to the loss of tissue homeostasis in peripheral organs, aggravating injury, and age-related pathological changes, thus shortening the life span of the body. Inflammaging causes pathophysiology changes of musculoskeletal system and promotes development and progression of osteoporosis and fractures, sarcopenia, and disorders of bone and mineral metabolism through regulating cell senescence, mitochondrial dysfunction, and immune aging.
This research topic aims to determine the mechanisms of how inflammaging promotes development and progression of osteoporosis and fractures, sarcopenia, and disorders of bone and mineral metabolism through regulating cell senescence, mitochondrial dysfunction, and immune aging.
The research topic welcomes basic and clinical original Research Article, Reviews, and Mini-reviews focusing on the following subtopics but are not limited to:
• Novel mechanisms of cell senescence, SASP, MiDAS and immune aging on pathophysiology changes of musculoskeletal system.
• Potential therapeutic molecules and small molecule peptides targeting cell senescence, SASP, MiDAS and immune aging for improving osteoporosis and fractures, sarcopenia, and disorders of bone and mineral metabolism through preventing cell senescence, mitochondrial dysfunction, and immune aging.
• Potential drugs for aging intervention to treat osteoporosis and fractures, sarcopenia, and disorders of bone and mineral metabolism by regulating inflammaging. Potential drugs for aging intervention include senolytics, sirtuin activator, mTOR inhibitor, AMPK activator, NAD+ precursors, NAD metabolism modulator, etc..
Inflammaging refers to the low level, chronic persistent and systemic inflammation of the body during aging without obvious infection, which is related to the chronic proinflammatory process of many aging-related diseases, and is a significant risk factor determining the incidence rate and mortality. The possible factors of inflammaging include cell senescence, mitochondrial dysfunction, and immune aging and so on. Cell senescence refers to the process of cell entering permanent cell cycle arrest. Aging cells have the characteristics of secreting senescence associated secretory phenotype (SASP) factors, including many proinflammatory factors, chemokines, growth factors and matrix degradation molecules, leading to changes of tissue microenvironment and cell biological function. Mitochondria dysfunction is a potential driver of inflammaging. With the gradual increase of mitochondria with dysfunction in the aging process, the autophagic clearance of mitochondria decreases, causing the increase of reactive oxygen species in mitochondria and the increase of dangerous associated molecular patterns from mitochondria, leading to the secretory phenotype of mitochondrial dysfunction associated senescence (MiDAS). Immune aging also plays a causal role in promoting inflammaging, leading to the loss of tissue homeostasis in peripheral organs, aggravating injury, and age-related pathological changes, thus shortening the life span of the body. Inflammaging causes pathophysiology changes of musculoskeletal system and promotes development and progression of osteoporosis and fractures, sarcopenia, and disorders of bone and mineral metabolism through regulating cell senescence, mitochondrial dysfunction, and immune aging.
This research topic aims to determine the mechanisms of how inflammaging promotes development and progression of osteoporosis and fractures, sarcopenia, and disorders of bone and mineral metabolism through regulating cell senescence, mitochondrial dysfunction, and immune aging.
The research topic welcomes basic and clinical original Research Article, Reviews, and Mini-reviews focusing on the following subtopics but are not limited to:
• Novel mechanisms of cell senescence, SASP, MiDAS and immune aging on pathophysiology changes of musculoskeletal system.
• Potential therapeutic molecules and small molecule peptides targeting cell senescence, SASP, MiDAS and immune aging for improving osteoporosis and fractures, sarcopenia, and disorders of bone and mineral metabolism through preventing cell senescence, mitochondrial dysfunction, and immune aging.
• Potential drugs for aging intervention to treat osteoporosis and fractures, sarcopenia, and disorders of bone and mineral metabolism by regulating inflammaging. Potential drugs for aging intervention include senolytics, sirtuin activator, mTOR inhibitor, AMPK activator, NAD+ precursors, NAD metabolism modulator, etc..
