As the core hub of energy metabolism in eukaryotes, mitochondria participate in a variety of cellular activities, including metabolic regulation of the cell matrix, apoptosis, and the activation of signal transduction pathways. Their functional status is closely linked to the initiation and progression of various diseases. Neurodegenerative diseases are primarily characterized by the progressive loss and dysfunction of neurons, and mitochondrial dysfunction is considered one of the key triggers in this process. The specific mechanisms by which mitochondrial dysfunction contributes to neurodegenerative diseases have attracted widespread attention. When misfolded or unfolded proteins are detected, a process known as the mitochondrial unfolded protein response (mtUPR) is activated to promote proper protein folding or degradation, thereby restoring mitochondrial function. As a mitochondrial stress defense mechanism, mtUPR primarily regulates the expression of nuclear-encoded genes, such as chaperones and proteases, to alleviate mitochondrial stress. Studies have shown that, in addition to misfolded and unfolded proteins, other mitochondrial stresses—such as mitochondrial DNA abnormalities and reactive oxygen species (ROS)—can also induce mtUPR. The biological functions of mtUPR extend beyond mitochondria and are crucial for the health of the entire cell and even the whole organism. The mtUPR process involves communication between mitochondria and the nucleus, a phenomenon that is highly conserved and has been observed across different species. Abnormal activation or inhibition of mtUPR is closely associated with the development of various neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease. An in-depth exploration of the dynamic regulatory role and molecular mechanisms of mtUPR is therefore of great significance for understanding the pathogenesis of these disorders. In addition to neuron loss, neurodegenerative diseases are characterized by the accumulation of misfolded proteins in the brain, including insoluble fibrils of amyloid beta, phosphorylated tau, or α-synuclein. While the molecular pathways of mtUPR are largely conserved across different diseases, the possibility of differential regulatory factors cannot be excluded. Although mtUPR activation is predominantly recognized for its cytoprotective role, it may exert deleterious effects when overstimulated or sustained. Chronic mtUPR activity has been linked to mitochondrial dysfunction and increased neuronal vulnerability, contributing to the pathogenesis of various neurodegenerative diseases. This review summarizes the fundamental concepts, major inducers, and signaling pathways of the mtUPR. We focus on the intrinsic relationship and regulatory patterns between mtUPR and neurodegenerative diseases, providing insights that may aid the development of targeted therapies. Finally, we discuss the challenges and future directions of mtUPR research in this field, aiming to pave the way for new therapeutic breakthroughs. A major limitation arises from the experimental models currently used; most findings rely on model organisms or cultured cells, which cannot fully replicate the complexity of human neurons. Future research should therefore focus on three main directions: (1) defining the molecular switches that determine whether mtUPR acts in a protective or detrimental manner; (2) elucidating differences in mtUPR molecular pathways across various models of neurodegenerative diseases; and (3) establishing robust biomarkers for mtUPR activity.

ObjectiveThe malaria parasites remodel the host erythrocyte structure by exporting parasite proteins that interact with the membrane skeleton proteins of red blood cells (RBCs), facilitating their intracellular survival and pathogenicity. Skeleton-binding protein 1 (SBP1) is a conserved exported protein across Plasmodium species. In Plasmodium falciparum, SBP1 has been reported to interact with erythrocyte membrane skeleton proteins 4.1R and spectrin, while its contribution to erythrocyte remodeling and parasite virulence in Plasmodium berghei (Pb) remains unclear. This study aims to determine whether PbSBP1 associates with the host cytoskeletal protein 4.1R and to investigate its role in the remodeling of host RBCs and the pathogenicity of Plasmodium berghei. MethodsIn Plasmodium berghei, the relationship between PbSBP1 and the erythrocyte cytoskeletal protein 4.1R was examined using co-immunoprecipitation. A Pbsbp1 gene knockout mutant of Plasmodium berghei (Pbsbp1∆) was generated based on the principle of double crossover homologous recombination. The deformability of erythrocytes infected with Pbsbp1∆ parasites was assessed using microfluidic methods. Microchannels with an array of cylindrical pillars were used to detect modifications in infected RBC deformability. The infected RBCs were squashed between the rows and recovered between the columns and the transit velocity (μm/s) of infected RBCs travelling through the microchannel was recorded. The component of the erythrocyte membrane skeleton junctional complex, tropomodulin (TMOD), was fluorescently labeled, and the cytoskeletal network of infected erythrocytes was imaged using super-resolution stochastic optical reconstruction microscopy (STORM) to analyze ultrastructural changes in the cytoskeleton of wild-type (WT) and Pbsbp1∆-infected erythrocytes. Actin-based junctional complexes were displayed as individual clusters by the labeled TMOD in the STORM images, and the cluster densities and distances between adjacent clusters of infected RBCs were calculated. Additionally, rodent malaria models (BALB/c mice) and experimental cerebral malaria models (C57BL/6 mice) were employed to monitor the growth of Pbsbp1∆ and WT parasites during the intraerythrocytic stage and their capacity to induce cerebral malaria in mice. ResultsPbSBP1 may participate in the remodeling of infected erythrocytes through direct or indirect interaction with the erythrocyte cytoskeletal protein 4.1R. Microfluidic assays revealed that the deformability of erythrocytes infected with Pbsbp1∆ parasites was significantly enhanced compared to those infected with WT parasites. STORM imaging further demonstrated that the ultrastructure of the erythrocyte cytoskeleton in Pbsbp1∆-infected cells was altered relative to that in WT-infected erythrocytes. The distances between nearest neighbors of clusters had a tendency to increase while the cluster densities were decreased in Pbsbp1∆-infected RBCs compared to WT-infected RBCs. Subsequent phenotypic analysis indicated that the growth rate of Pbsbp1∆ parasites during the intraerythrocytic stage was significantly slower than that of WT parasites, and their ability to induce cerebral malaria in mice was also attenuated. These findings suggest that PbSBP1 is involved in the remodeling of the erythrocyte membrane skeleton, likely through its direct or indirect interaction with protein 4.1R, thereby regulating the deformability of infected erythrocytes and influencing the pathogenicity of the blood-stage parasites. ConclusionThis study establishes a role for PbSBP1 in host erythrocyte remodeling and parasite virulence, providing new research strategies for the prevention and treatment of malaria.

OBJECTIVE To formulate Guidelines for the standardized implementation of pharmacist-managed clinics （ 2026 edition ） in response to the challenges faced by such clinics in China， including uneven development， large discrepancies in service specifications， insufficient patient awareness， and limited medical insurance coverage. METHODS Led by the Pharmaceutical Affairs Professional Committee of the Chinese Hospital Association， the Evidence-based Pharmacy Professional Committee of the Chinese Pharmaceutical Association， and the Hospital Pharmacy Professional Committee of the Cross-strait Medical and Health Exchange Association， a total of 19 domestic hospital pharmacy experts were organized. Through a systematic review of national policies and literature research， current practical experience was summarized. Consensus on the contents of the guidelines was reached after in-depth discussions. RESULTS &CONCLUSIONS The guidelines covered five sections： definition and connotation of pharmacist-managed clinics， establishment requirements， implementation and management， post competency， and practical research. Firstly， the definition and connotation included three operational forms of pharmacist-managed clinics （independent mode， physician-pharmacist joint mode， and online pharmacist-managed clinic mode） and classified service modes （specialty-specific， drug-specific， and disease-specific pharmacist-managed clinics）. The establishment requirements were further refined， covering system construction （pharmaceutical service management system， quality control and assessment mechanism）， personnel qualifications （professional credentials， continuing education and professional training， etc）， service recipients， as well as service venues and facilities. Subsequently， the implementation and management of pharmacist-managed clinics were proposed， involving service procedures， intervention measures， documentation and records， patient education and follow-up， humanistic care， as well as risk management and quality control. Finally， post competency encompassed the competency requirements for pharmacists providing services in pharmacist-managed clinics， as well as the suggestions on teaching methods； practical research encouraged the conduct of high-quality pharmaceutical practice in the setting of pharmacist-managed clinics. The guidelines provide valuable guidance for the standardized implementation of pharmacist-managed clinics in China in terms of establishment， management， teaching， and research， fill the guideline gap in this field， and can promote the high-quality development of pharmacist-managed clinics.

OBJECTIVE To provide standardized guidance for the rational clinical use of antibody-based drugs for the treatment of myasthenia gravis， and to enhance the evidence-based system of guidelines and consensus in this field. METHODS The consensus expert team consisted of 71 multidisciplinary experts from 28 provinces/autonomous regions/municipalities directly under the Central Government. Evidence was systematically retrieved through multiple databases， drug package inserts， and official websites of international and national health administrative authorities， drug regulatory agencies， healthcare security departments， and related industry associations， up to April 30， 2025. Evidence was graded according to the 2014 version of JBI pre-grading system for evidence from intervention studies. Based on full consideration of the current best evidence and multidisciplinary expert experience， the expert consensus recommendations were formulated using a modified Delphi method. RESULTS The Evidence-based expert consensus on the clinical application and pharmaceutical management of antibody-based drugs for the treatment of myasthenia gravis standardized the key points of whole-process pharmaceutical management for four antibody-based drugs approved for marketing in the mainland of China for the treatment of myasthenia gravis （efgartigimod alfa， efgartigimod alfa/hyaluronidase， eculizumab， and rozanolixizumab）. It formulated 37 expert consensus recommendations covering nine pharmaceutical management aspects： drug suitability selection， medication in special populations， administration methods， drug storage， therapeutic drug monitoring and pharmacogenetic testing， immunization management， drug interactions， pharmaceutical care， and off-label drug use. CONCLUSIONS Based on the current best evidence and multidisciplinary expert experience， this consensus establishes a whole-process management framework for antibody-based drugs for the treatment of myasthenia gravis， from clinical application to pharmaceutical management. It provides a scientific basis for the rational and precise use of these drugs in clinical practice， effectively promotes the enhancement of pharmaceutical management efficiency， and helps improve the overall therapeutic benefits for patients.

Chronic obstructive pulmonary disease （COPD） is a chronic respiratory disease that poses a significant threat to global health， exhibiting high morbidity， disability and mortality rate， with its prevention and treatment situation becoming increasingly critical. The pathogenesis of COPD is complex， and the underlying cellular and molecular biological mechanisms remain incompletely elucidated. Programmed cell death （PCD） is the process wherein cells actively undergo demise to maintain internal environmental stability in response to certain signals or specific stimuli. Contemporary medical research indicates that the dysregulation of PCD patterns such as apoptosis， necroptosis， pyroptosis， autophagy， and ferroptosis is closely related to the onset and progression of COPD. Clarifying the molecular mechanisms of PCD in COPD may provide novel perspectives for in-depth understanding and prevention of the disease. Traditional Chinese medicine （TCM） is characterized by holistic regulation. In recent years， extensive research has been conducted in the TCM field focusing on modulating apoptosis， necroptosis， pyroptosis， autophagy， and ferroptosis for the treatment of COPD， yielding remarkable achievements. Therefore， this study systematically explored the molecular mechanism of PCD in COPD and reviewed the potential mechanisms and intervention status of TCM targeting PCD in COPD， aiming to provide insights and references for the clinical prevention， treatment and in-depth research of COPD.

Chronic obstructive pulmonary disease （COPD） is a chronic respiratory disease that poses a significant threat to global health， exhibiting high morbidity， disability and mortality rate， with its prevention and treatment situation becoming increasingly critical. The pathogenesis of COPD is complex， and the underlying cellular and molecular biological mechanisms remain incompletely elucidated. Programmed cell death （PCD） is the process wherein cells actively undergo demise to maintain internal environmental stability in response to certain signals or specific stimuli. Contemporary medical research indicates that the dysregulation of PCD patterns such as apoptosis， necroptosis， pyroptosis， autophagy， and ferroptosis is closely related to the onset and progression of COPD. Clarifying the molecular mechanisms of PCD in COPD may provide novel perspectives for in-depth understanding and prevention of the disease. Traditional Chinese medicine （TCM） is characterized by holistic regulation. In recent years， extensive research has been conducted in the TCM field focusing on modulating apoptosis， necroptosis， pyroptosis， autophagy， and ferroptosis for the treatment of COPD， yielding remarkable achievements. Therefore， this study systematically explored the molecular mechanism of PCD in COPD and reviewed the potential mechanisms and intervention status of TCM targeting PCD in COPD， aiming to provide insights and references for the clinical prevention， treatment and in-depth research of COPD.

To explore the advantages of traditional Chinese medicine （TCM） and integrative TCM-Western medicine approaches in the treatment of diabetic microvascular complications （DMC）， refine key pathophysiological insights and treatment principles， and promote academic innovation and strategic research planning in the prevention and treatment of DMC. The 38th session of the Expert Salon on Diseases Responding Specifically to Traditional Chinese Medicine， hosted by the China Association of Chinese Medicine， was held in Beijing， 2024. Experts in TCM， Western medicine， and interdisciplinary fields convened to conduct a systematic discussion on the pathogenesis， diagnostic and treatment challenges， and mechanism research related to DMC， ultimately forming a consensus on key directions. Four major research recommendations were proposed. The first is addressing clinical bottlenecks in the prevention and control of DMC by optimizing TCM-based evidence evaluation systems. The second is refining TCM core pathogenesis across DMC stages and establishing corresponding "disease-pattern-time" framework. The third is innovating mechanism research strategies to facilitate a shift from holistic regulation to targeted intervention in TCM. The fourth is advancing interdisciplinary collaboration to enhance the role of TCM in new drug development， research prioritization， and guideline formulation. TCM and integrative approaches offer distinct advantages in managing DMC. With a focus on the diseases responding specifically to TCM， strengthening evidence-based support and mechanism interpretation and promoting the integration of clinical care and research innovation will provide strong momentum for the modernization of TCM and the advancement of national health strategies.

ObjectiveTo analyze the research status and development trends of non-pharmacological therapies for post-stroke spasticity (PSS) over the past two decades. MethodsRelevant literatures on non-pharmacological rehabilitation of PSS published from January, 2004 to June, 2024 were retrieved from Web of Science Core Collection. CiteSpace 6.3.R6 and VOSviewer 1.6.18 were used for visualization analysis. ResultsA total of 780 publications were included. The annual number of publications showed an overall upward trend. China, the USA, and Italy contributed the highest number of publications. The Hong Kong Polytechnic University and researcher Noureddin Nakhostin Ansari were identified as the most influential institution and author, respectively. High-frequency keywords and cluster labels included electric stimulation, transcranial magnetic stimulation, robot and acupuncture. ConclusionOver the past 20 years, researches on non-pharmacological therapies for PSS have remained active, with hotspots focusing on diverse interventions such as electrical stimulation, magnetic stimulation and robot-assisted therapy.

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock is the primary cause of mortality in sepsis, with its core pathophysiological mechanism being severe ischemia and hypoxia in critical units—composed of microcirculation and the mitochondria of functional cells—resulting from disruptions in blood flow and oxygen flow following a dysregulated host response. Due to the systemically convergent yet clinically heterogeneous nature of the host response, current understanding and management strategies for hemodynamics remain inconsistent, often leading to inadequate resuscitation or overtreatment. To improve the quality of care, based on a systematic review of the "blood flow-oxygen flow" theory, an expert panel emphasizes reevaluating septic shock from an integrated perspective of blood flow and oxygen flow, and has formulated the Expert Consensus on Blood Flow and Oxygen Delivery Phenotyping and Clinical Management of Septic Shock (2025). The consensus proposes that clinical typing of blood flow-oxygen flow should comprehensively consider cardiac function, vascular tone, oxygen flow utilization status in critical units, and disease trajectory, while optimizing subtype identification by integrating host response phenotypes and artificial intelligence technologies. It advocates establishing a continuous assessment system through multi-site oxygen flow monitoring for organ perfusion, peripheral perfusion monitoring, and critical care ultrasound. Under the framework of the "critical care triangle", the consensus promotes the implementation of individualized, bundled management strategies, providing guidance for multiple management points to restore blood flow-oxygen flow matching, reduce the risk of organ failure, and decrease patient mortality.

OBJECTIVE To provide a basis for aligning Chinese pharmacoeconomic research on heart failure （HF） with international standards. METHODS A qualitative comparison o f domestic and global HF pharmacoeconomic studies was conducted across four dimensions： research methods and model application， research perspectives and endpoints， data sources and parameter selection， and policy translation and practical impact. RESULTS & CONCLUSIONS Global studies predominantly utilize long-term dynamic models， societal perspectives， real-world data integration， and directly inform reimbursement decisions. Conversely， domestic research often relies on short-term simplified models， a single healthcare system perspectives， literature-derived data， and individual medicine recommendations. Future domestic studies should transition to long-term dynamic modeling， develop localized disease-specific utility databases via big data， establish reimbursement-linked closed-loop mechanisms， and foster multidisciplinary collaboration to optimize healthcare resource allocation.