Ferroptosis is a non-apoptotic form of cell death that integrates metabolic disorders, oxidative stress, and inflammation, characterized by the accumulation of iron-dependent lipid peroxidation. A growing body of literature suggests that ferroptosis is involved in the pathogenesis of chronic respiratory diseases. In addition, there is a notable association between ferroptosisrelated genes and molecules and chronic respiratory diseases, indicating their potential as disease biomarkers. This article summarizes the research progress on the role of ferroptosis in chronic respiratory diseases, discusses the advances in existing therapies targeting ferroptosis in chronic respiratory diseases, and highlights the main obstacles in translating experimental research into clinical applications, with the aim of providing new insights for the treatment of chronic respiratory diseases.

Pulmonary hypertension (PH) is a severe disease characterized by pulmonary vascular remodeling and functional impairment, ultimately leading to right heart failure and high mortality rates. Ion channels, particularly calcium, potassium, and sodium channels, play crucial roles in the pathogenesis of PH. These ion channels regulate the activity of smooth muscle cells through various pathways, influencing vascular contraction, cell proliferation, and inflammatory responses. The dysregulation of these physiological and pathological processes plays a pivotal role in the onset and progression of PH. This article aims to comprehensively review the role and mechanisms of ion channels in the pathogenesis of PH, explore their potential as therapeutic targets, and provide a theoretical basis for developing novel treatment strategies for PH.

Circular RNAs (circRNAs), as endogenous non-coding RNAs, are prevalent in the transcriptomes of eukaryotes and regulate various aspects of organisms' life activities, including transcriptional regulation, epigenetic modification, signal transduction, and chromatin modification. These regulatory functions are closely and indispensably linked to a wide range of diseases. In recent years, with circRNA research deepened gradually, circRNAs related to pulmonary hypertension have been increasingly identified, making them a new focus in the current study of pulmonary hypertension pathogenesis. This article presents an overview of the current research status of circRNAs in the field of pulmonary arterial hypertension, elucidating their functional roles and mechanisms underlying the disease.

Chronic obstructive pulmonary disease (COPD) is one of the most common respiratory diseases, clinically characterized by persistent airflow limitation and chronic respiratory symptoms such as dyspnea, cough, and sputum production. Currently, COPD has become the third leading cause of death worldwide, exhibiting high prevalence, high mortality, and a significant disease burden, making its prevention and control a critical public health challenge. The concept of the "gut-lung axis" provides novel insights into the pathogenesis of COPD, as well as its clinical prevention and treatment. The gut microbiota refers to the collective microorganisms residing in the intestinal tract, which play a vital role in maintaining host immunity and metabolic homeostasis. Recent studies have demonstrated the essential role of the gut microbiota in COPD pathogenesis. On one hand, the composition and functionality of the gut microbiota are perturbed in patients and rodents with COPD. On the other hand, gut microbiota derived from COPD patients can induce similar symptoms to those of the disease, whereas restoring the gut microbiota can at least partially delay the progression of COPD and alleviate its symptoms. This review summarizes the latest findings regarding the gut microbiota in COPD, particularly the role of gut microbiota in COPD pathogenesis and its underlying mechanisms, providing new insights into the future investigations, diagnosis and treatment of COPD.

The diaphragm is the main respiratory muscle, and its activity can be used to assess respiratory muscle function. Diaphragm function can be evaluated by its electrical activity (diaphragm electromyography, EMGdi) and mechanical functions such as pleural pressure reflected by esophageal pressure. Compared with esophageal pressure, EMGdi recorded by a multipair esophageal electrode catheter could serve as a more reliable biomarker of neural respiratory drive. The pathophysiological changes of various respiratory diseases including obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease are related to neural respiratory drive. Accurately recording EMGdi and quantifying neural respiratory drive has become an important tool for exploring disease pathogenesis and aiding in diagnosis. This article introduces the method for recording EMGdi and quantifying neural respiratory drive using a multipair esophageal electrode catheter, summarizing its value in the diagnosis and treatment of chronic respiratory diseases.

Epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase and a member of the ErbB family. It is widely expressed in various tissues and organs of the human body, including the skin, lungs, liver, and kidneys. EGFR regulates intracellular homeostasis by activating key signaling pathways such as JAK/STAT、MAPK/ERK, and PI3K/AKT. Furthermore, EGFR modulates disease processes by participating in immune and inflammatory responses following activation by growth factors and G protein-coupled receptors. Recent studies have shown that EGFR is associated with most pulmonary diseases, such as lung cancer, chronic obstructive pulmonary disease, bronchial asthma, and pneumonia. Therefore, this article reviews recent advances in EGFR research related to pulmonary diseases.

Exosomes play an important role in intercellular communication by transferring substances such as proteins, lipids and nucleic acids between cells. The types and quantities of substances carried by exosomes vary depending on their cellular origin, resulting in heterogeneity in both the characteristics and functions of exosomes derived from different cell types. This heterogeneity underpins the basis of exosome function. Focusing on the heterogeneity of exosomes in terms of cellular origin and content, this article systematically elucidates the biological characteristics and functions of exosomes, providing a basis for future exosome screening and applications.

Peroxisome proliferator-activated receptor-γ coactivator 1-α (PGC1α) is a crucial regulator of mitochondrial biogenesis and oxidative metabolism, with its activity and expression linked to various diseases. In recent years, there has been a growing body of research on the relationship between PGC1α and cancer. The role of PGC1α in tumors exhibits significant heterogeneity, with both overexpression and underexpression of PGC1α reported to be associated with tumor occurrence, development, and prognosis, emphasizing its critical role in tumorigenesis and progression. Therefore, this article comprehensively reviews the classification, structure, function, activity regulation, and pro-carcinogenic and anti-carcinogenic effects of PGC1α, as well as its roles in oral cancer, aiming to provide a valuable theoretical reference for targeted energy metabolism therapy of malignant tumors.

Sphingosine-1-phosphate (S1P), a metabolite of cell membrane sphingolipids, exerts its physiological functions by binding to G protein-coupled sphingosine-1-phosphate receptors (S1PRs) in various tissues of the human body. The S1P-S1PR signaling pathway plays a crucial role in mediating inflammatory responses, cardiac development, angiogenesis, as well as the migration, proliferation, and differentiation of immune cells. S1PRs have emerged as promising therapeutic targets for a variety of diseases, including autoimmune diseases, inflammation, cardiovascular diseases, and even cancer. However, the lack of in-depth understanding of S1PRs has hindered the development of clinical drugs. Therefore, this article reviews the current research status of S1PRs, focusing on S1PR-associated physiological functions, disease progression, and the development of representative drugs, with the aim of providing new insights for the clinical treatment of associated diseases.

Metabolites produced by the gut microbiota play various physiological regulatory roles through interactions with the host and are closely related to human health. Imidazole propionate, a metabolite derived from histidine by the gut microbiota, has garnered significant attention in recent years due to its close association with chronic diseases such as type 2 diabetes and cardiovascular diseases. This article reviews the metabolic pathways of imidazole propionate, its correlation with metabolic and cardiovascular diseases, its mechanisms of action, and current methods for its detection and associated interventions. The aim is to provide a reference for the prevention and control of chronic diseases targeting imidazole propionate.

Hypoxic pulmonary hypertension (HPH) is a key pathophysiological change in chronic pulmonary heart disease and various types of high-altitude diseases,which can ultimately lead to right ventricular failure and even death.Its pathogenesis mainly includes hypoxic pulmonary vasoconstriction and pulmonary vascular remodeling.Pulmonary arterial smooth muscle cells (PASMCs) are the main arterial cells that constitute the pulmonary artery wall,and their hypertrophy and proliferation are significant pathological features of HPH structural remodeling. Therefore,exploring the proliferative status of PASMCs is a core research area in pulmonary vascular structural remodeling.The glucose - 6- phosphate dehydrogenase (G6PD) pathway has emerged as one prominent focus both domestically and internationally. Intervening in PASMCs remodeling in HPH by inhibiting G6PD can reverse HPH. To better understand the relationship between the pathogenesis of HPH and the G6PD pathway, this review focuses on the research progress concerning the role of G6PD in regulating hypoxia-induced metabolic shifts and proliferation in PASMCs. The aim is to provide novel perspectives for the clinical treatment of HPH.

Sarcopenia is an age-related, systemic skeletal muscle disease that severely affects the health and quality of life of the elderly, serving as one of the leading causes of disability and increased social burden among this population. The imbalance between protein synthesis and degradation is a primary pathogenic mechanism, in which the ubiquitin-proteasome system (UPS), particularly E3 ubiquitin ligases (E3s), plays a crucial role in regulating muscle protein degradation. This article elucidates and summarizes the impact and mechanisms of E3s in sarcopenia-associated muscle atrophy, aiming to provide novel insights for basic research, the identification of therapeutic targets, and the development of preventive strategies for sarcopenia.

Post-stroke cognitive impairment (PSCI) is a common complication following stroke, posing a significant threat to patients' quality of life and survival time. Microglia, the major immune cells in the central nervous system, play a crucial role in the pathogenesis of PSCI by mediating immune responses and exerting neuroprotective effects. Research has indicated that triggering receptor expressed on myeloid cells 2 (TREM2), an immune response receptor predominantly expressed on microglia, is involved in the regulation of microglial number, phagocytosis, cytokine release, and metabolic functions. In this article, we elucidate the effect of TREM2-mediated regulation of microglial activity on PSCI, and explore the potential of TREM2 as a therapeutic target for the prevention and treatment of PSCI.