Senescent immune cells release grancalcin to promote skeletal aging

Li, Changjun; Xiao, Ye; Sun, Yu‐Chen; He, Wenzhen; Liu, Ling; Huang, Mei; He, Chen; Huang, Min; Chen, Kaixuan; Hou, Jing; Xu, Feng; Su, Tian; Guo, Qi; Huang, Yan; Peng, Hui; Yang, Mingzhi; Liu, Guanghui; Luo, Xiang‐Hang

doi:10.1016/j.cmet.2021.08.009

Cited by 109 publications

(105 citation statements)

References 62 publications

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“…Mechanisms underlying senescent induced changes in MSCs have since then been addressed in multiple studies, identifying important mediators of MSC senescence [ 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 ]. For instance, several miRNAs have been identified that are involved in regulating senescence and the balance between osteoblastic and adipocytic differentiation of BMSCs [ 52 , 55 , 60 , 61 ].…”

Section: Cellular Senescencementioning

confidence: 99%

Section: Cellular Senescencementioning

confidence: 99%

“…In a very recent study Li et al [ 63 ] provide evidence for the accumulation of proinflammatory and senescent subtypes of immune cells in the bone marrow of aging rats and mice. These cells were shown to secrete granalcin, which in turn represses osteogenesis and promotes adipogenesis [ 63 ], thereby underlining the crucial interplay between the immune system and senescence in promoting age-related phenotypes. In another study Guo et al [ 62 ] support a link between the accumulation of advanced glycation end products (AGEs) and BMSCs senescence by suggesting Sirt3-mediated mitophagy as regulatory mechanism of this process.…”

Section: Cellular Senescencementioning

confidence: 99%

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Age Related Osteoporosis: Targeting Cellular Senescence

Föger-Samwald

Kerschan‐Schindl

Butylina

et al. 2022

IJMS

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Age-related chronic diseases are an enormous burden to modern societies worldwide. Among these, osteoporosis, a condition that predisposes individuals to an increased risk of fractures, substantially contributes to increased mortality and health-care costs in elderly. It is now well accepted that advanced chronical age is one of the main risk factors for chronical diseases. Hence, targeting fundamental aging mechanisms such as senescence has become a promising option in the treatment of these diseases. Moreover, for osteoporosis, the main pathophysiological concepts arise from menopause causing estrogen deficiency, and from aging. Here, we focus on recent advances in the understanding of senescence-related mechanisms contributing to age-related bone loss. Furthermore, treatment options for senile osteoporosis targeting senescent cells are reviewed.

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Section: Cellular Senescencementioning

confidence: 99%

Section: Cellular Senescencementioning

confidence: 99%

Section: Cellular Senescencementioning

confidence: 99%

See 1 more Smart Citation

Age Related Osteoporosis: Targeting Cellular Senescence

Föger-Samwald

Kerschan‐Schindl

Butylina

et al. 2022

IJMS

View full text Add to dashboard Cite

show abstract

“…Osteoporosis-related fractures are becoming more prevalent in the elderly and result in a series of problems and a higher mortality risk. There is a strong association between ageing and osteoporosis ( Li et al, 2021 ). New approaches to osteoporosis treatment have resulted from research on the fundamental mechanisms of bone resorption and production ( Compston et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

The Role of Senescence-Associated Secretory Phenotype in Bone Loss

Zhu

Wan

Yang

et al. 2022

Front. Cell Dev. Biol.

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As the population of most nations have a large proportion of older individuals, there is an increase in the prevalence of osteoporosis. Consequently, scientists have focused their attention on the pathogenic mechanisms of osteoporosis. Owing to an increase in studies on cellular senescence in recent years, research has begun to focus on the function of the senescent microenvironment in osteoporosis. With chronic inflammation, senescent cells in the bone marrow secrete a series of factors known as senescence-associated secretory phenotype (SASP) factors, acting on their own or surrounding healthy cells and consequently exacerbating ageing.The components of the SASP may differ depending on the cause of osteoporosis. This review aimed to summarize the relationship between SASP factors and osteoporosis and suggest new insights into the mechanistic investigation of osteoporosis.

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“…The excessive triglycerides accumulation in the liver during MAFLD might lead to pro-inflammatory and anti-inflammatory factor imbalance, affecting the function of immune cells whose homeostasis is largely influenced by their metabolic activities [ 13 ]. Thus, specific metabolic adaptability should be acquired to support their diverse immune functions [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

The Imbalance of Mitochondrial Homeostasis of Peripheral Blood-Derived Macrophages Mediated by MAFLD May Impair the Walking Ability of Elderly Patients with Osteopenia

Wang

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

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Introduction. Many Asian cohort studies have shown that nonalcoholic fatty liver disease (NAFLD), now renamed as metabolic dysfunction-associated fatty liver disease (MAFLD), increases the risk of osteoporosis, yet the effect of MAFLD on elderly patients with osteopenia (OPe) has not been reported. Objective. This study aimed to explore the influence of MAFLD on the function of macrophages in patients with OPe. Methods. A total of 107 elderly OPe patients with or without MAFLD who visited the Huadong Hospital Affiliated to Fudan University (Shanghai, China) between January 1st, 2021, and September 30th, 2021, were evaluated for an interviewer-assisted questionnaire, as well as clinical and biological assessments. Results. Comparing two groups of elderly patients with the same bone mass level, we found that the six-minute walking distance ( P = 0.012 ) and short physical performance battery (SPPB) score ( P = 0.0029 ) of the elderly OPe patients with MAFLD are worse than those in OPe patients without MAFLD. Our results confirmed that the mitochondrial reactive oxygen species (mtROS) in peripheral blood of OPe patients with MAFLD was significantly higher than those without. We also observed the mitochondrial metabolism level of peripheral blood-derived macrophages in the included patients and peripheral blood macrophages in patients with MAFLD with more unbalanced mitochondrial dynamics of macrophages, more weakened mitochondrial respiratory capacity, and greater mitochondrial microstructure damage, when compared with the elderly patients without MAFLD. Conclusions. To conclude, our data revealed that MAFLD itself may aggravate the inflammatory state in elderly OPe people due to mitochondrial homeostasis imbalance of peripheral blood macrophages. Damaged monocyte-macrophages might trigger attenuation of the walking ability of OPe patients.

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Senescent immune cells release grancalcin to promote skeletal aging

Cited by 109 publications

References 62 publications

Age Related Osteoporosis: Targeting Cellular Senescence

Age Related Osteoporosis: Targeting Cellular Senescence

The Role of Senescence-Associated Secretory Phenotype in Bone Loss

The Imbalance of Mitochondrial Homeostasis of Peripheral Blood-Derived Macrophages Mediated by MAFLD May Impair the Walking Ability of Elderly Patients with Osteopenia

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