Pharmacological Reviews最新文献

{"title":"Medication adherence: An overlooked critical determinant of pharmacological effectiveness.","authors":"Michel Burnier, Michel Azizi, Pankaj Gupta, Przemyslaw Kardas, Marie-Paule Schneider, Bernard Vrijens","doi":"10.1016/j.pharmr.2026.100161","DOIUrl":"https://doi.org/10.1016/j.pharmr.2026.100161","url":null,"abstract":"<p><p>Medication adherence and therapeutic inertia are 2 major barriers to the optimal control of chronic diseases in clinical practice. In drug development, these factors contribute to variability in drug exposure and may substantially influence estimates of efficacy, safety, and benefit-risk balance, but they frequently remain overlooked. Medication adherence is a complex and dynamic process characterized by several patterns and a large number of determinants that may exert variable, phase-specific, and time-dependent effects throughout the medication-taking process. A major challenge remains the accurate monitoring of drug adherence, the ideal goal being that of obtaining a reliable dosing history and confirmation that the medication has been taken as prescribed. Several new approaches discussed in this review are available to monitor adherence in clinical studies with more precision, but their implementation remains limited. This review discusses contemporary approaches to improve patients' medication adherence and to limit physicians' inertia, another form of poor adherence. Among them, interprofessional collaborations have demonstrated sustained improvements in adherence and therapeutic inertia. However, this approach still needs profound changes in terms of interprofessional education and collaboration and strong support from teaching organizations and health care providers. Finally, our review addresses an often overlooked issue in drug development, eg, the need to consider the entire drug life cycle from chemical development to the accumulation and disposal of drugs when unused. Medication nonadherence is now recognized as a significant driver of pharmaceutical waste and environmental burden. Modern clinical pharmacology should consider the global environmental impact of drugs. SIGNIFICANCE STATEMENT: Medication adherence and therapeutic inertia are 2 major determinants of variable drug exposure but they remain insufficiently recognized and systematically addressed. This review examines the taxonomy, the multiple determinants of nonadherence and therapeutic inertia, the various methods available to measure adherence, and some innovative approaches for designing future clinical trials that account for these 2 variables. Finally, we address an increasingly important but often overlooked consequence of poor medication adherence: the environmental and economic impact of unused medicines.</p>","PeriodicalId":19780,"journal":{"name":"Pharmacological Reviews","volume":"78 6","pages":"100161"},"PeriodicalIF":20.3,"publicationDate":"2026-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances in methotrexate pharmacology and potential therapeutic uses in age-related cardiometabolic and neurodegenerative diseases.","authors":"Arduino A Mangoni, Julie-Ann Hulin, Sara Tommasi","doi":"10.1016/j.pharmr.2026.100147","DOIUrl":"10.1016/j.pharmr.2026.100147","url":null,"abstract":"<p><p>Experimental and clinical evidence continues to accumulate, supporting the critical role of dysregulated inflammation, immunity, and redox signaling in the pathophysiology of various age-related cardiometabolic and neurodegenerative diseases. While ongoing research is investigating novel anti-inflammatory and immunomodulatory therapies for such conditions, available antirheumatic drugs may serve a similar purpose. One such drug, methotrexate, has been successfully used at high doses since the 1940s as an anticancer agent and, more recently, at lower doses in patients with autoimmune diseases. Although the effects of methotrexate have traditionally been attributed to its antiproliferative activity via folic acid modulation, additional targets have been identified, including AMP-activated protein kinase, Janus kinase/signal transducer and activator of transcription, high mobility group box 1 protein, the gut microbiota, and additional pharmacological effects of adenosine, a key mediator of methotrexate. The beneficial effects of modulating these targets on downstream inflammatory and immune pathways, cellular senescence, and vascular, metabolic, and brain homeostasis have been increasingly investigated in experimental models. Furthermore, studies conducted over the past 20 years suggest an association between low-dose methotrexate and a decreased risk of certain age-related cardiometabolic and neurodegenerative diseases, particularly in patients with autoimmune conditions. The results of these studies support the potential protective role of methotrexate against age-associated cardiometabolic and neurodegenerative diseases through multiple mechanisms, unlike targeted immunomodulatory and anti-inflammatory drugs, thereby providing a robust framework for investigating its repurposing in future intervention studies. SIGNIFICANCE STATEMENT: New treatments are essential to address the burden of age-related diseases. The important roles of dysregulated inflammation, immunity, and redox signaling in these conditions have spurred research into developing new therapies or repurposing existing drugs to target these dysfunctions. The disease-modifying antirheumatic drug methotrexate has shown potential protective effects against cellular senescence and certain age-related cardiometabolic and neurodegenerative diseases. This knowledge will encourage further research into the repurposing of methotrexate for the treatment of these diseases.</p>","PeriodicalId":19780,"journal":{"name":"Pharmacological Reviews","volume":"78 5","pages":"100147"},"PeriodicalIF":20.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hunting gremlins: GREM1 as a new therapeutic target for multiple diseases including glaucoma.","authors":"David P Siderovski, Nishanth Myneni, Monica Botross, Pinkal D Patel, Abbot F Clark","doi":"10.1016/j.pharmr.2026.100152","DOIUrl":"10.1016/j.pharmr.2026.100152","url":null,"abstract":"<p><p>The transforming growth factor-β (TGF-β) superfamily of signaling molecules is involved in normal development and homeostasis. However, aberrant signaling among members of the TGF-β superfamily plays an important pathogenic role in numerous diseases. Increased expression of the pleiotropic cytokine and growth factor TGF-β leads to aberrant signaling associated with numerous diseases, including fibrosis of multiple tissues, a wide variety of cancers, obesity and diabetes, and glaucoma, among others. Normally, the profibrotic effects of TGF-β are regulated by concurrent signaling through bone morphogenetic proteins (BMPs). Unfortunately, many disease states exhibit increased expression of the BMP antagonist Gremlin-1 (GREM1), which suppresses this protective effect of BMPs. Targeting TGF-β is challenging as a therapeutic target because TGF-β is still needed for basal signaling required for normal tissue/cell functions. GREM1 is a more attractive therapeutic target because its expression in most tissues is limited after development. However, targeting GREM1 has been very challenging and long considered an \"undruggable\" target. Fortunately, several new approaches, including the discovery of GREM1-directed aptamers, proteolysis targeting chimera small molecules, and neutralizing antibodies, as well as the design of protein-protein interaction inhibitors, are being explored to directly target and inhibit GREM1 pathogenic functions and activities, thereby restoring homeostasis. SIGNIFICANCE STATEMENT: Gremlin-1 (GREM1) is a secreted bone morphogenetic protein antagonist re-expressed in numerous diseases fibrosis, glaucoma, and cancer. Once deemed \"undruggable,\" GREM1 has recently become a validated therapeutic target, exemplified by the current clinical development of GREM1-neutralizing antibodies. Additional experimental strategies represent promising, although still preclinical, approaches to suppress GREM1 activity or enhance its degradation, offering new avenues to restore transforming growth factor-β/bone morphogenetic protein signaling balance in disease.</p>","PeriodicalId":19780,"journal":{"name":"Pharmacological Reviews","volume":"78 5","pages":"100152"},"PeriodicalIF":20.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148888327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Promise of Biased Ligands in Therapeutics","authors":"Dylan S. Eiger,Jeffrey S. Smith,Sudarshan Rajagopal","doi":"10.1016/j.pharmr.2026.100160","DOIUrl":"https://doi.org/10.1016/j.pharmr.2026.100160","url":null,"abstract":"","PeriodicalId":19780,"journal":{"name":"Pharmacological Reviews","volume":"158 1","pages":"100160"},"PeriodicalIF":21.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148895655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peptide hormone-based combinational pharmacotherapies for chronic metabolic diseases.","authors":"Zara Siu Wa Chui, Yaqian Xue, Xiaoping Wu, Aimin Xu","doi":"10.1016/j.pharmr.2026.100150","DOIUrl":"10.1016/j.pharmr.2026.100150","url":null,"abstract":"<p><p>Peptide hormones play a central role in maintaining metabolic homeostasis by integrating complex signaling pathways to coordinate interorgan crosstalk. Aberrant production and/or dysfunction of peptide hormones are important contributors to the pathophysiology of a cluster of interrelated chronic metabolic diseases (CMDs), including obesity, type 2 diabetes mellitus, dyslipidemia, metabolic dysfunction-associated steatotic liver disease, and cardiovascular diseases. These CMDs often co-occur, ranking among the top causes of death and disability in the rapidly aging population. Peptide hormone-based pharmacotherapies are the mainstay of treatment for these CMDs. Analogs and agonists of peptide hormones produced by classical endocrine cells, especially insulin and glucagon-like peptide-1, are cornerstones in managing diabetes and obesity. Furthermore, peptide hormones released from nonclassical endocrine organs, such as liver-secreted fibroblast growth factors 21 and growth differentiation factor 15, have emerged as highly promising therapeutic candidates for obesity-related metabolic comorbidities. These peptide hormones act synergistically and/or complementarily to exert pleiotropic metabolic benefits through their distinct receptors in different target organs/tissues. Combination pharmacotherapies with these peptide hormones are much more effective than monotherapy and hold promise to address the multimorbidity issue in patients with CMDs. This review summarizes recent advances in the pharmacoengineering and pharmacology of these peptide hormone-based long-acting analogs and coagonists and discusses their synergistic and antagonistic interactions in the treatment of CMDs. Furthermore, we highlight major challenges and future perspectives in the clinical development of multiple peptide hormone-based coagonists as safe and effective pharmacotherapy for the management of metabolic comorbidities. SIGNIFICANCE STATEMENT: This review highlights recent clinical advances in combination peptide hormone therapies for chronic metabolic diseases, emphasizing their superior efficacy over monotherapies in addressing metabolic multimorbidity. Summarizing the latest developments in long-acting analogs and coagonists of peptide hormones provides critical insights into their synergistic mechanisms, clinical potential, and future challenges, offering a comprehensive perspective for improving the management of complex metabolic disorders.</p>","PeriodicalId":19780,"journal":{"name":"Pharmacological Reviews","volume":"78 5","pages":"100150"},"PeriodicalIF":20.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148606197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic pain in Alzheimer disease and the role of neuroimmune interactions.","authors":"Marzia Malcangio, George Sideris-Lampretsas","doi":"10.1016/j.pharmr.2026.100149","DOIUrl":"10.1016/j.pharmr.2026.100149","url":null,"abstract":"<p><p>Chronic pain conditions affect a large proportion of the global population and pain has tremendous personal and economic impact, affecting quality of life and ability to work while imposing a significant burden on families and health care systems. Neurological disorders and painful conditions are frequently accompanied by chronic pain, which is often jointly diagnosed with age-related neurodegenerative diseases, however, many patients do not receive adequate treatment. This review aims to create a working framework around the issue of under-recognized/undertreated chronic pain in Alzheimer disease by offering an in-depth overview of the mechanisms driving chronic pain and how we can leverage this knowledge to advance therapeutics approaches for these patients with an emphasis on the immune system. SIGNIFICANCE STATEMENT: Chronic pain conditions are prevalent among the aging population, and they positively associate with dementia. The incidence of chronic pain is associated with neuropsychiatric symptoms of dementia and pain management should aim for effective treatments regardless of cognitive status.</p>","PeriodicalId":19780,"journal":{"name":"Pharmacological Reviews","volume":"78 5","pages":"100149"},"PeriodicalIF":20.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148584897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploration of multifunctional characteristics and regulatory mechanism of promoter G-quadruplexes.","authors":"Ziyi Zhao, Yangzi Zhang, Jingjing Tian, Yuan Su, Shenghao Lin, Keren Chen, Longjiao Zhu, Wentao Xu","doi":"10.1016/j.pharmr.2026.100151","DOIUrl":"10.1016/j.pharmr.2026.100151","url":null,"abstract":"<p><p>G-quadruplexes (G4s), a specialized nucleic acid secondary structure, have been found in recent years to be widely distributed in gene promoter regions. Growing evidence has highlighted the significance of G4 structures of promoter region in regulating various biological processes, including transcription and epigenetic regulation. In this review, we first proposed the 8 main characteristics of G-quadruplexes in the promoter region: widespread distribution, positional specificity, structural diversity, precise regulation, genetic modifiability, dynamic reversibility, signal responsiveness, and synergistic regulation. Common G4 regulators were then categorized as natural products, transcription factors and other binding proteins, small molecule ligands, and nucleic acids, which were fully summarized. Then different types of characterization methods for promoter region G4 and its ligands are summarized. Finally, the directions of promoter region G4 applications, including disease diagnosis, bioimaging, synthetic biology, targeted therapies, and antiviral potentials, which have been the focus of recent studies, are sorted out and presented. SIGNIFICANCE STATEMENT: Promoter G-quadruplexes (G4s) are emerging as dynamic and multifunctional regulatory elements that shape transcription, epigenetic states, and cellular responses to environmental cues. By pioneering the definition of 8 key features and corresponding regulatory mechanisms, this review highlights their significant potential as novel targets for therapeutic intervention and provides a comprehensive framework that advances both fundamental understanding and translational exploration of promoter G4s in disease diagnosis, imaging, synthetic biology, and targeted therapy.</p>","PeriodicalId":19780,"journal":{"name":"Pharmacological Reviews","volume":"78 5","pages":"100151"},"PeriodicalIF":20.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148471988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Renal aging and associated diseases: Common mechanisms and therapeutic approaches.","authors":"Jabir Aliyu Muhammad, Nadya Marcelina Julianto, Tania Setiawan, Teresa Fiona Fadjaray, Fernando Elbert, Mudasir Hussain, Lawrence Mario Wirawan, Dongjun Jeong, Hyog Young Kwon","doi":"10.1016/j.pharmr.2026.100148","DOIUrl":"10.1016/j.pharmr.2026.100148","url":null,"abstract":"<p><p>The kidneys are highly metabolically active organs that undergo a progressive, intrinsic decline in renal function with aging, a process that can be further exacerbated by chronic exposure to oxidative stress, inflammation, hypertension, and various toxins. Studies have shown that the prevalence of acute kidney injury and chronic kidney disease is significantly higher in the elderly. This suggests that the age-related reduction in baseline renal function, rather than advanced age itself, increases the susceptibility to and severity of these disorders after nephrotoxic insults. We comprehensively discuss the emerging recognition of shared molecular and cellular mechanisms underpinning fibrosis and cellular senescence, 2 hallmark features of functional decline seen in renal aging, acute kidney injury, and chronic kidney disease, as well as proposing the interconnection between these events. Furthermore, we highlight therapeutic strategies aimed at mitigating kidney damage and counteracting the effects of aging. These include lifestyle modifications, small-molecule inhibitors, and senotherapeutic approaches such as senolytics and senomorphics. Overall, this work aims to establish a foundation for understanding the pathogenesis of renal aging and related diseases, while also identifying promising avenues for effective therapeutic intervention. SIGNIFICANCE STATEMENT: Cellular senescence and fibrosis intersect in renal aging, acute kidney injury, and chronic kidney disease, highlighting shared pathways that may be targeted to slow disease progression and providing insights into the underlying mechanisms, current interventions, and future strategies for age-related kidney disorders.</p>","PeriodicalId":19780,"journal":{"name":"Pharmacological Reviews","volume":"78 5","pages":"100148"},"PeriodicalIF":20.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148536547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GPCR signaling from a primary cilium perspective.","authors":"Olof Idevall-Hagren, Jing Hughes","doi":"10.1016/j.pharmr.2026.100159","DOIUrl":"https://doi.org/10.1016/j.pharmr.2026.100159","url":null,"abstract":"<p><p>G protein-coupled receptors (GPCRs) are best known for initiating signaling at the plasma membrane, yet a substantial and functionally distinct subset of these receptors localizes to the primary cilium, a highly specialized cell-surface organelle. Over the past decade, the primary cilium has emerged as a privileged signaling compartment that concentrates GPCRs, signaling effectors, and second messengers within a physically constrained and biochemically unique environment. In this review, we synthesize current knowledge of GPCR signaling from a primary cilium perspective, with emphasis on receptor repertoire, trafficking mechanisms, and compartment-specific signal transduction. We discuss how ciliary entry and exit are regulated by dedicated transport systems, how canonical GPCR signaling components-G proteins, GPCR kinases, β-arrestins, regulators of G protein signaling, and A-kinase anchoring proteins-are organized within cilia, and how the ciliary geometry, membrane composition, voltage, pH, and cytoskeletal architecture shape signaling outcomes. We further highlight how cilia support autonomous and highly sensitive microdomains of cAMP and calcium (Ca²⁺) signaling, enabling integration and hierarchical control of multiple GPCR inputs. Finally, we examine the physiological consequences of ciliary GPCR signaling in neural, renal, adipose, and pancreatic and developmental tissues, where defects in ciliary signaling contribute to metabolic disease, impaired morphogenesis, and tissue homeostasis, and ciliopathies-a range of human disorders arising from primary cilium dysfunction. Together, these studies establish the primary cilium as a dynamic and modular GPCR signaling hub and underscore the importance of subcellular localization in determining receptor function and signaling specificity. SIGNIFICANCE STATEMENT: Beyond their traditional role at the plasma membrane, many GPCRs signal from primary cilia, specialized cellular compartments that create unique signaling environments. This review synthesizes advances in ciliary GPCR trafficking, organization, and signal transduction, showing how subcellular localization determines receptor function and how disrupted ciliary signaling contributes to human diseases, including ciliopathies, metabolic disorders, and developmental defects.</p>","PeriodicalId":19780,"journal":{"name":"Pharmacological Reviews","volume":"78 6","pages":"100159"},"PeriodicalIF":20.3,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149063660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Harnessing autophagy and its transcriptional regulation in tumorigenesis and neurodegeneration: Potential and existing therapeutic strategies.","authors":"Parul Suri, Abel B Daartey, D M Isha Olive Khan, Naga Pradeep Rayana, Rameswari Chilamakuri, Deepika Godugu, Mahan Gholam Azad, Katelyn L Reeb, Des R Richardson","doi":"10.1016/j.pharmr.2026.100158","DOIUrl":"https://doi.org/10.1016/j.pharmr.2026.100158","url":null,"abstract":"<p><p>Autophagy is a fundamental cellular process that maintains homeostasis by degrading and recycling cellular components. As autophagy is essential for metabolizing damaged organelles and toxic substances, it plays a crucial role in both normal physiology and pathological conditions. However, autophagy has dual roles in both tumorigenesis and neurodegeneration. In cancer, autophagy can act as a tumor suppressor by clearing damaged components in early stages, but promotes tumor survival and growth in later stages, particularly under stress. In neurodegeneration, impaired autophagy is implicated in the disease progression of conditions such as Alzheimer, Parkinson, and Huntington diseases, in which the failure to clear misfolded proteins and damaged organelles exacerbates disease pathology. This review is organized to cover the molecular machinery and transcriptional regulation of autophagy, its disease-specific subtypes, its dual roles in tumorigenesis and neurodegeneration, and the current pharmacological landscape for therapeutic targeting. Attention is given to pharmacological modulation of autophagy, including senolytic drugs that selectively eliminate senescent cells by exploiting their dependence on antiapoptotic survival pathways, and small-molecule regulators targeting key pathways such as phosphoinositide 3-kinase/Akt serine/threonine kinase/mechanistic target of rapamycin and AMP-activated protein kinase. Depending on the pathological context, these drugs are under development to either inhibit or induce autophagy. Additionally, we address the challenges and limitations in developing effective autophagy-targeting drugs, underscoring the need for further research to identify new compounds that can modulate cellular autophagic flux. SIGNIFICANCE STATEMENT: Autophagy is an important homeostatic mechanism, and its dysregulation contributes to a wide range of diseases, including cancer and neurodegenerative disorders. Therefore, a deeper mechanistic understanding of the regulation of autophagy is crucial for advancing targeted therapies with significant clinical impact.</p>","PeriodicalId":19780,"journal":{"name":"Pharmacological Reviews","volume":"78 6","pages":"100158"},"PeriodicalIF":20.3,"publicationDate":"2026-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149207567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}