Fan Yu

From a mechanical stimulation perspective, this study aims to explore the mechanisms by which dance training affects bone metabolism and to clarify its potential as a preventive and therapeutic measure for osteoporosis (OP). A comprehensive search was conducted on the PubMed, Web of Science, and China National Knowledge Infrastructure databases, utilizing search terms related to dance, mechanical stimulation, and OP. The present study incorporated a wide range of research methodologies, including randomized controlled trials, observational studies, systematic reviews, and narrative reviews, with the overarching objective of encompassing all pertinent concepts within the purview of our investigation. The synthesis and description of the search results were conducted through a narrative approach. A preliminary investigation of extant literature suggests that studies that comprehensively delineate the mechanism of action between dance and OP are few and far between. However, a thorough review of the extant literature indicates that dance training can enhance bone density and promote skeletal health by influencing mechanical characteristics. Concurrently, dance can function as a mechanical stimulus, thereby regulating bone metabolism by activating relevant cellular signaling pathways, thus contributing to the reduction of bone loss. Dance training, as a form of mechanical stimulation, has the potential to play a crucial role in the prevention and treatment of OP. However, the precise nature of the dance styles, the training intensities and frequencies remains unclear. It is recommended that future research endeavors concentrate on the comprehensive integration of these measures, with the objective of addressing the existing knowledge gaps. This approach is expected to provide a more robust evidence base for the utilization of dance-based strategies in the prevention and management of OP.

Heart failure represents the terminal stage in the development of many cardiovascular diseases, and its pathological mechanisms are closely related to disturbances in energy metabolism and mitochondrial dysfunction in cardiomyocytes. In recent years, nicotinamide adenine dinucleotide (NAD⁺), a core coenzyme involved in cellular energy metabolism and redox homeostasis, has been shown to potentially ameliorate heart failure through the regulation of mitochondrial function. This review systematically investigates four core mechanisms of mitochondrial dysfunction in heart failure: imbalance of mitochondrial dynamics, excessive accumulation of reactive oxygen species (ROS) leading to oxidative stress injury, dysfunction of mitochondrial autophagy, and disturbance of Ca²⁺ homeostasis. These abnormalities collectively exacerbate the progression of heart failure by disrupting ATP production and inducing apoptosis and myocardial fibrosis. NAD⁺ has been shown to regulate mitochondrial biosynthesis and antioxidant defences through the activation of the deacetylase family (e.g., silent information regulator 2 homolog 1 (SIRT1) and SIRT3) and to increase mitochondrial autophagy to remove damaged mitochondria, thus restoring energy metabolism and redox balance in cardiomyocytes. In addition, the inhibition of NAD⁺-degrading enzymes (e.g., poly ADP-ribose polymerase (PARP), cluster of differentiation 38 (CD38), and selective androgen receptor modulators (SARMs)) increases the tissue intracellular NAD⁺ content, and supplementation with NAD⁺ precursors (e.g., β-nicotinamide mononucleotide (NMN), nicotinamide riboside, etc.) also significantly elevates myocardial NAD⁺ levels to ameliorate heart failure. This study provides a theoretical basis for understanding the central role of NAD⁺ in mitochondrial homeostasis and for the development of targeted therapies for heart failure.

Estrogen levels are the core factor influencing postmenopausal osteoporosis (PMOP). Estrogen can affect the progression of PMOP by regulating bone metabolism, influencing major signaling pathways related to bone metabolism, and modulating immune responses. When estrogen levels decline, the activity of Sirtuins (SIRTs) is reduced. SIRTs are enzymes that function as NAD+-dependent deacetylases. SIRTs can modulate osteocyte function, sustain mitochondrial homeostasis, and modulate relevant signaling pathways, thereby improving bone metabolic imbalances, reducing bone resorption, and promoting bone formation. In PMOP, SIRT1, SIRT3, and SIRT6 are primarily affected. Oxidative stress (OS) is a crucial factor in PMOP, as it generates excessive reactive oxygen species (ROS) that exacerbate PMOP. There is a certain interplay between SIRTs and OS. The reduced activity of SIRTs leads to intensified OS and the excessive accumulation of ROS. In return, ROS suppresses the AMPK signaling pathway and the synthesis of NAD+, which consequently diminishes the function of SIRTs. Natural SIRT activators and natural antioxidants, which are characterized by high safety, convenience, and minimal side effects, represent a potential therapeutic strategy for PMOP. This study aims to investigate the mechanisms of SIRTs and OS in PMOP and summarize potential therapeutic strategies to assist in the improvement of PMOP.

Perimenopausal women have fluctuating estrogen levels, which often trigger a range of symptoms of perimenopausal syndromes as estrogen levels decrease. Changes in perimenopausal estrogen levels are closely related to pain in knee osteoarthritis (KOA), which has long been a research area of great interest in perimenopausal women. In recent years, it has been found that perimenopausal estrogen levels have an important role in KOA pain, namely, that estrogen can affect KOA pain through the regulation of inflammatory responses, inhibition of cellular senescence and apoptosis, and modulation of neurotransmitters, which may provide new ideas for KOA treatment. This study aims to describe the mechanism of estrogen level on knee osteoarthritis pain in perimenopause and related non-pharmacological measures, such as physical therapy, physical factor therapy, traditional Chinese medicine, and diet, which can provide a reference for the study and treatment of pain in perimenopausal women with KOA.

Osteoarthritis (OA) is a chronic, progressive degenerative joint disease that affects the entire synovial joint, leading to the progressive degeneration of articular cartilage. It seriously affects the quality of life and global disability of patients. OA is affected by a variety of factors; the most significant risk factor for OA is age. As individuals age, the risk and severity of OA increase due to the exacerbation of cartilage degeneration and wear and tear. In recent years, research has indicated that the gut microbiota may play a significant role in the aging and OA processes. It is anticipated that regulating the gut microbiota may offer novel approaches to the treatment of OA. The objective of this paper is to examine the relationship between the gut microbiota and senile OA, to investigate the potential mechanisms involved. This review also summarizes the therapeutic strategies related to gut flora in OA management, such as prebiotics and probiotics, diet, exercise, traditional Chinese medicine (TCM) modification, and fecal microbiota transplantation (FMT), highlighting the potential clinical value of gut flora and elucidating the current challenges. The foundation for future research directions is established through the summarization of current research progress.