Xuejuan Xu

As the global population ages, the risks associated with primary sarcopenia, including falls, fractures, functional decline, and frailty, are becoming increasingly apparent, all of which significantly impair the quality of life in older adults. Emerging evidence suggests that the gut microbiota plays a pivotal role in maintaining muscle physiology. Specific gut bacteria promote intramuscular protein synthesis through the production of certain amino acids (e.g., leucine, tryptophan), short-chain fatty acids (SCFAs), and hydrogen sulfide. Notably, Escherichia coli expressing the enzyme nicotinamidase (PncA) has been shown to enhance nicotinamide adenine dinucleotide (NAD+) synthesis, potentially improving mitochondrial function in muscle tissue. Furthermore, secondary bile acids and lactate influence the levels of fibroblast growth factor 15/19 and unacylated ghrelin in circulation by binding to receptors that are highly expressed in gut endocrine cells, thereby affecting muscle physiology. This review examines the characteristic composition of the gut microbiota in patients with sarcopenia, its role in primary sarcopenia, and potential therapeutic targets.

There is currently a lack of pathological research on the hair loss caused by stress, and there is no effective treatment available. It has been previously reported that stress can cause sympathetic nerve activation and release of norepinephrine, which binds to beta‐2 adrenergic receptors and causes a series of chemical reactions. Propranolol, as a beta‐2 adrenergic receptors blocker, competitively antagonizes the effects of norepinephrine. We initiated a single‐center clinical trial with a self‐controlled approach to assess the effectiveness of topical applied hydrochloride salt of propranolol solution in preventing stress‐induced hair loss in humans. A total of 20 volunteers were enrolled. 14 out of 20 volunteers experienced a significant reduction in the number of hair loss ( p < .05) after using hydrochloride salt of propranolol solution. No local adverse reactions were found. This study showed hydrochloride salt of propranolol solution may alleviate stress‐induced alopecia to a certain extent, which provides clues for the development of pharmaceutical interventions for the treatment of stress‐induced alopecia.

Hair follicle (HF) homeostasis is regulated by various signaling pathways. Disruption of such homeostasis leads to HF disorders, such as alopecia, pigment loss, and hair aging, which is causing severe health problems and aesthetic concerns. Among these disorders, hair aging is characterized by hair graying, hair loss, hair follicle miniaturization (HFM), and structural changes to the hair shaft. Hair aging occurs under physiological conditions, while premature hair aging is often associated with certain pathological conditions. Numerous investigations have been made to determine the mechanisms and explore treatments to prevent hair aging. The most well-known hypotheses about hair aging include oxidative stress, hormonal disorders, inflammation, as well as DNA damage and repair defects. Ultimately, these factors pose threats to HF cells, especially stem cells such as hair follicle stem cells, melanocyte stem cells, and mesenchymal stem cells, which hamper hair regeneration and pigmentation. Here, we summarize previous studies investigating the above mechanisms and the existing therapeutic methods for hair aging. We also provide insights into hair aging research and discuss the limitations and outlook.

Although the gut microbiota has been reported to influence osteoporosis risk, the individual species involved, and underlying mechanisms, remain largely unknown. We performed integrative analyses in a Chinese cohort of peri-/post-menopausal women with metagenomics/targeted metabolomics/whole-genome sequencing to identify novel microbiome-related biomarkers for bone health. Bacteroides vulgatus was found to be negatively associated with bone mineral density (BMD), which was validated in US white people. Serum valeric acid (VA), a microbiota derived metabolite, was positively associated with BMD and causally downregulated by B. vulgatus. Ovariectomized mice fed B. vulgatus demonstrated increased bone resorption and poorer bone micro-structure, while those fed VA demonstrated reduced bone resorption and better bone micro-structure. VA suppressed RELA protein production (pro-inflammatory), and enhanced IL10 mRNA expression (anti-inflammatory), leading to suppressed maturation of osteoclast-like cells and enhanced maturation of osteoblasts in vitro. The findings suggest that B. vulgatus and VA may represent promising targets for osteoporosis prevention/treatment.

The skin is a multi‐layered structure composed of the epidermis, dermis and hypodermis. The epidermis originates entirely from the ectoderm, whereas the dermis originates from various germ layers depending on its anatomical location; thus, there are different developmental patterns of the skin. Although the regulatory mechanisms of epidermal formation are well understood, mechanisms regulating dermis development are not clear owing to the complex origin. It has been shown that several morphogenetic pathways regulate dermis development. Of these, transforming growth factor‐β (TGF‐β) and fibroblast growth factor (FGF) signalling pathways are the main modulators regulating skin cell induction, fate decision, migration and differentiation. Recently, the successful generation of human skin by modulating TGF‐β and FGF signals further demonstrated the irreplaceable roles of these pathways in skin regeneration. This review provides evidence of the role of TGF‐β and FGF signalling pathways in the development of different skin layers, especially the disparate dermis of different body regions. This review also provides new perspectives on the distinct developmental patterns of skin and explores new ideas for clinical applications in the future.

Chronic and acute stress caused by emotional or physical insults can affect the function of other organs via the brain‐body axis. As one of the smallest organs in mammalian, hair follicles are highly susceptible to stress. Under stress, the sympathetic nerves release norepinephrine (NA), which acts directly on the β‐2 adrenergic receptors on melanocyte stem cells (MeSCs) within the hair follicles, causing the MeSCs to lose quiescence and enter a rapid proliferation state followed by differentiation and migration, leading to rapid loss of MeSCs and, ultimately, grey hair. Here, we screened out β‐2 blockers forming the ZINC 15 compound database, found a natural product isoliensinine, and was effective in preventing stress‐induced hair greying in mice. The study sheds light on the development of products that use natural compounds to prevent stress‐induced hair greying.

Sarcopenia is an age‐related accelerated loss of muscle strength and mass. Bone and muscle are closely related as they are physically adjacent, and bone can influence muscle. However, the temporal association between bone mineral density (BMD) and muscle mass in different regions of the body after adjustment for potential indicators and the mechanisms by which bone influences muscle in sarcopenia remain unclear. Therefore, this study aimed to explore the temporal association between muscle mass and BMD in different regions of the body and mechanisms by which bone regulates muscle in sarcopenia. Here, cross‐lagged models were utilized to analyze the temporal association between BMD and muscle mass. We found that low‐density lipoprotein (LDL‐C) positively predicted appendicular lean mass. Mean whole‐body BMD (WBTOT BMD), lumbar spine BMD (LS BMD), and pelvic BMD (PELV BMD) temporally and positively predicted appendicular lean mass, and appendicular lean mass temporally and positively predicted WBTOT BMD, LS BMD, and PELV BMD. Moreover, this study revealed that primary mice femur osteoblasts, but not primary mice skull osteoblasts, induced differentiation of C2C12 myoblasts through exosomes. Furthermore, the level of long noncoding RNA (lncRNA) taurine upregulated 1 (TUG1) was decreased, and the level of lncRNA differentiation antagonizing nonprotein coding RNA (DANCR) was increased in skull osteoblast–derived exosomes, the opposite of femur osteoblast–secreted exosomes. In addition, lncRNA TUG1 enhanced and lncRNA DANCR suppressed the differentiation of myoblasts through regulating the transcription of oxidative stress–related myogenin (Myog) gene by modifying the binding of myogenic factor 5 (Myf5) to the Myog gene promoter via affecting the nuclear translocation of Myf5. The results of the present study may provide novel diagnostic biomarkers and therapeutic targets for sarcopenia.