Short-chain fatty acids (SCFAs) are produced by the gut microbiota through the fermentation of dietary fibers, which include acetic acid, propionic acid, and butyric acid. These SCFAs regulate various physiological functions in the body, such as immune, metabolic, and neurological functions, and are considered key factors affecting host health. SCFAs contribute to promoting lactate metabolism, increasing glycogen storage, and improving intestinal barrier function, thereby enhancing exercise performance. However, different types of SCFAs exhibit variations in their mechanisms of action and effects. This review discusses how SCFAs synthesized by the gut microbiota influence exercise performance and the underlying mechanisms, providing new insights and directions for the use of SCFAs derived from the gut microbiota to improve exercise performance.

Traumatic brain injury (TBI) is defined as functional alterations or other pathological changes in the brain caused by external forces, which is a significant public health issue worldwide. Currently, a large number of studies have proved that exercise, as a nonpharmacological treatment, can effectively improve TBI. Exercise both before and after injury can benefit TBI recovery through specific mechanisms. This article summarizes the effects of exercise before and after injury on TBI and their potential regulatory mechanisms, aiming to provide an in-depth understanding of the mechanisms through which exercise improves TBI, thereby offering a theoretical basis for the clinical application of exercise in the prevention and treatment of TBI.

Coronavirus disease-19 (COVID-19) is a disease mainly characterized by respiratory symptoms caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Research evidence has indicated that regular exercise plays an important role in preventing COVID-19, enhancing therapeutic effectiveness, and avoiding adverse prognosis. This article reviews the effects and mechanisms of exercise before, during and after the prevention and treatment of COVID-19. Exercise plays its role through regulating the ACE2/Ang(1-7)/Mas axis, enhancing immunity and cardiopulmonary function, inhibiting inflammatory factors and oxidative stress, regulating intestinal flora homeostasis, and improving psychological well-being. Additionally, we summarize the exercise prescriptions for different stages of COVID-19 prevention and treatment. By comprehensively summarizing the role of exercise in the prevention and treatment of COVID-19, we also aim to provide references for the prevention and treatment of similar respiratory infectious diseases in the post-pandemic era.

Inflammatory bowel disease (IBD) is a chronic intestinal inflammatory disease represented by Crohn's disease (CD) and ulcerative colitis (UC). Mechanisms underlying its onset and development involve genetic susceptibility, as well as multiple pathways such as the environmental and microbial interactions that weaken the intestinal barrier and lead to immune activation. Recent research has indicated that triggering receptors expressed on myeloid cells (TREMs) expressed on macrophages play critical roles in both innate and adaptive immune responses, closely associated with the occurrence and development of IBD. This article reviews the structures, ligands, and functions of TREM-1/2 (TREM-1 and TREM-2), as well as mechanisms underlying the involvement of TREM-1/2 in IBD and the accompanying mental disorders, aiming to provide theoretical support for the prevention and treatment of IBD.

Cardiometabolic disease (CMD) refers to the single or simultaneous occurrence of pathological changes in the metabolic and cardiovascular systems that can mutually influence each other, which is a collective term for metabolic and cardiovascular diseases,including obesity,insulin resistance,metabolic syndrome,diabetes,and coronary heart disease, etc. Adipokines play a critical role in the occurrence and development of CMD. Complement C1q TNF-related protein 7 (CTRP7) is a recently discovered adipokine closely associated with CMD, such as obesity, diabetes and coronary heart disease. Focusing on the biological characteristics of CTRP7, this article reviews its role in the occurrence and development of CMD, including obesity, type 2 diabetes mellitus and coronary heart disease, as well as the possible mechanisms such as regulating glucose and lipid metabolism, decreasing insulin sensitivity, promoting inflammatory responses and increasing oxidative stress, so as to provide evidence and references for CTRP7 as a therapeutic target of CMD.

Triggering receptor expressed on myeloid cells 2 (TREM2) is a transmembrane receptor belonging to the immunoglobulin superfamily. It is primarily expressed on myeloid cells and microglia. Upon binding to its ligand, TREM2 activates downstream signaling pathways through the intracellular adaptor protein DAP12/DAP10, playing an important role in immune signaling. TREM2 is involved in the regulation of various biological processes, including phagocytosis, inflammatory reactions, and metabolic processes. Its significant role has been observed in the onset and development of various diseases. Recent research has highlighted the key role of TREM2 in the development of malignant tumors. Apart from regulating the biological behavior of tumor cells, TREM2 can also modulate the activity and function of immune cells within the tumor microenvironment, contributing to the formation of a suppressive immune microenvironment. This article aims to summarize the regulatory role of TREM2 in different types of malignant tumors and provide prospects for future research related to targeted therapies involving TREM2, thereby offering novel insights for research in the field of cancer prevention and treatment.

Atherosclerosis (AS) is a chronic inflammatory vascular disease and the main pathological basis for numerous cardiovascular and cerebrovascular diseases. The pathogenesis of AS is complex and not yet fully elucidated. Vascular smooth muscle cells (VSMCs) are one of the main cell types that constitute the vascular wall. They are involved in regulating the systolic and diastolic functions of the vascular wall and maintaining the vascular tone. However, under the stimulation of AS promoting factors, the phenotypic switch occurs in systolic VSMCs, exhibiting characteristics such as proliferation, migration, adhesion, and calcification, which may directly lead to the formation or rupture of AS plaques. Integrins play a critical role in coordinating the transmembrane connections between the extracellular matrix and cytoskeleton, contributing to pathological processes of various diseases. They also play key roles in regulating the transdifferentiation of VSMCs into mesenchymal stem cells, myofibroblasts, macrophages, osteoblasts, and other cell types. To conclude, integrins can indirectly affect the formation and progression of AS by regulating the phenotypic transformation of VSMC, thereby presenting the potential as a new therapeutic target for AS. In this article, we review the classification of VSMC phenotypic transformation and the regulatory role of integrins in VSMC phenotypic transformation, aiming to provide new targets and strategies for the early treatment and intervention of AS.

Exosomes are a subtype of extracellular vesicles derived from endosomes and released by membrane fusion and exocytosis. Exosome-mediated intercellular communication plays a critical role in multiple physiological and pathological processes. Due to their low immunogenicity and ability to mediate long-distance transport of bioactive substances, exosomes are considered ideal biological carriers for drugs. Engineered exosomes can improve the targeting of drug delivery, making research on exosome-based drug delivery exceedingly promising. However, some studies have indicated that exosomes can facilitate pathological processes in diseased organisms. For instance, exosomes secreted by tumor cells can "mislead" immune cells or establish a favorable microenvironment, thus promoting tumor proliferation and migration. In neurodegenerative diseases, exosomes exacerbate the disease by promoting inflammatory responses and the spread of pathogenic proteins. This article reviews the development and pathological propagation of neurodegenerative diseases mediated by exosomes carrying toxic pathogenic proteins , offering new insights into the occurrence and development of neurodegenerative diseases, as well as cautions and recommendations for exosome engineering and clinical applications.

Mechanotransduction occurs when tissues or cells are stimulated by external mechanical forces, initiating a series of signaling processes, with mechanosensitive ion channels playing a pivotal role in this signaling cascade. Among these channels, Piezo1 has been widely studied. Piezo1 has been found in a variety of mammalian tissues and can affect multiple signaling pathways after mechanical stimulation, involving processes such as vasodilation, cell migration, and inflammatory response. To explore the potential therapeutic value of Piezo1 and improve the understanding of its function, this article reviews literature on Piezo1 and summarizes the latest research progress on Piezo1 in the cardiovascular system, locomotor system, nervous system, respiratory system, digestive system, and reproductive system.

Non-alcoholic fatty liver disease (NAFLD) and sarcopenia are common age-related chronic comorbidities that share many common pathophysiological factors. However, their underlying mechanisms have not been fully elucidated. In recent years, cuproptosis has been discovered as a new cell death mode, and the potential functional role of copper homeostasis in a variety of chronic diseases has become a research focus. Loss of copper in the liver is closely related to the occurrence of early NAFLD, and copper overload in skeletal muscles may promote the occurrence of sarcopenia through various signaling pathways. As indicated by ceruloplasmin levels in serum, extracellular copper overload may play a potential functional role in this process. This review discusses the possible mechanism of copper homeostasis imbalance and the onset of early NAFLD combined with sarcopenia from the perspective of copper metabolism, in order to provide molecular targets and theoretical basis for early clinical improvement or even reversal of these two metabolic diseases.

Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic non-infectious liver disease nationwide that can progress to liver cirrhosis and liver cancer, posing a significant threat to human health. Under hypoxic conditions at high altitudes, various organs and systems of the body are affected. Liver tissues, in particular, experience intensified hypoxia, leading to a significantly higher prevalence of NAFLD in plateau areas than in sea level areas. Currently, there are diverse opinions on the pathogenesis of NAFLD, and the specific mechanisms by which high-altitude hypoxia promotes NAFLD progression remain unclear. In this article, we review the impact of high-altitude hypoxia on liver parenchymal cells and mesenchymal cells, consolidate relevant research findings, and summarize the potential mechanisms by which high-altitude hypoxia may contribute to the progression of chronic NAFLD, providing new insights for the prevention and treatment of NAFLD.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel coronavirus that primarily affects the lungs and causes coronavirus disease 2019 (COVID-19). Recent clinical cases have reported the cardiovascular complications of COVID-19, including myocarditis, arrhythmia, myocardial infarction, and so on. Among them, COVID-19-related myocarditis exhibits diverse symptoms, which can occur at different ages and has a delayed onset. Moreover, COVID-19-related myocarditis is positively correlated with the poor prognosis and mortality of COVID-19 patients. The exploration of its clinical characteristics, potential pathogenesis and treatment may provide new ideas and strategies for the prevention and drug development of COVID-19-related myocarditis in the future. This article provides an overview of both domestic and foreign researches on COVID-19-related myocarditis.

N6-methyladenosine (m6A), which belongs to the field of the epigenetic modifications, is a common and reversible mRNA modification in eukaryotic RNA. Regulated by methyltransferases, demethyltransferases, and reader proteins, m6A modification affects the expression of relevant proteins by mediating RNA transcription, splicing, translation, and other processes, thereby regulating the physiological and biochemical processes of the organism. Major depressive disorder (MDD), characterized by a high incidence, low cure rate, and a high recurrence rate, is a psychiatric disorder with multiple etiological factors, including genetic factors, environmental factors and epigenetic factors. However, the specific mechanisms underlying MDD remain unclear. Recent studies have found a close relationship between m6A modification and the pathogenesis of MDD, making it a hot topic in MDD research. This article reviews the m6A methylation, as well as the expression and roles of related enzymes in the central nervous system of MDD patients, aiming to provide new insights and potential drug targets for the research and treatment of MDD.