MedComm - Future medicine最新文献

{"title":"Biomarkers in Glaucoma: From Diagnosis to Future Therapeutic Strategies","authors":"Shruthi Merugu,&nbsp;Janhvi Vyas,&nbsp;Govind Soni,&nbsp;Khushwant S. Yadav","doi":"10.1002/mef2.70073","DOIUrl":"https://doi.org/10.1002/mef2.70073","url":null,"abstract":"<p>Glaucoma is a chronic neurodegenerative disease and one of the leading causes of irreversible blindness worldwide. Although intraocular pressure (IOP) remains the major modifiable risk factor, visual loss may continue despite adequate IOP control, indicating the need for improved approaches to diagnosis and treatment. Current clinical methods have limited sensitivity for detecting early neuronal injury and predicting disease progression. Increasing evidence suggests that molecular alterations related to oxidative stress, neurodegeneration, and immune dysfunction occur before clinically detectable structural changes in the glaucomatous eye. These early changes may provide useful biomarkers for early diagnosis, assessment of disease activity, prediction of progression, and treatment selection. Advances in analytical techniques and data-driven approaches have further expanded the potential for translating biomarker research into clinical practice. This review summarizes current evidence on glaucoma biomarkers and evaluates their potential clinical relevance for prognosis and treatment. Particular emphasis placed on biomarkers that may support neuroprotective and IOP-independent therapeutic strategies. Integration of biomarker-based approaches with precision medicine may facilitate earlier detection, improved monitoring, and more individualized management of glaucoma, with the potential to improve long-term visual outcomes.</p>","PeriodicalId":74135,"journal":{"name":"MedComm - Future medicine","volume":"5 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mef2.70073","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149146531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GABAergic TH2 Amacrine Cells Participate in Spontaneous Wave Activity in the Developing Retina","authors":"Wenqiu Wang,&nbsp;Heather E. Durfee,&nbsp;Yasmeen Hassan,&nbsp;Stephanie M. Bumbaru,&nbsp;Anthony J. Barbu,&nbsp;Alycen Wiacek,&nbsp;Dao-Qi Zhang","doi":"10.1002/mef2.70075","DOIUrl":"https://doi.org/10.1002/mef2.70075","url":null,"abstract":"<p>Amacrine cells (ACs) are retinal interneurons that play essential roles in object motion detection, contrast sensitivity, and light adaptation. A subtype of GABAergic ACs identified in a tyrosine hydroxylase (TH) promoter-driven green fluorescent protein (GFP) transgenic mouse line, termed TH2 amacrine cells (TH2 ACs), has recently been implicated in the feature selectivity of object-motion signals in the adult retina. However, the functional properties and developmental roles of TH2 ACs remain largely unknown. Here, we demonstrate that TH2 ACs exhibit spontaneous rhythmic depolarizations during early postnatal retinal development. During the first postnatal week, these depolarizations are driven by cholinergic input from starburst amacrine cells (SACs). In the second postnatal week, spontaneous rhythmic activity persists but is mediated by glutamatergic input from bipolar cells. Calcium imaging further revealed that this spontaneous activity propagates across the TH2 AC network as retinal waves, potentially generating spatially and temporally patterned GABA release. Pharmacological experiments indicate that GABAergic signaling from TH2 ACs could contribute to the inhibitory regulation of the spatiotemporal properties of spontaneous retinal waves. Together, these findings identify TH2 ACs as active components of developing retinal wave circuits and suggest that they may contribute to the activity-dependent refinement of retinal circuitry underlying object-motion processing.</p>","PeriodicalId":74135,"journal":{"name":"MedComm - Future medicine","volume":"5 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mef2.70075","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149146534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond Proteolysis-Targeting Chimeras: Endoplasmic-Reticulum-Associated Degradation-Engaging Chimeras Ensure Targeted Degradation of Membrane Proteins","authors":"Jinping Huang,&nbsp;Yalan Wu,&nbsp;Xiaolong Tang","doi":"10.1002/mef2.70074","DOIUrl":"https://doi.org/10.1002/mef2.70074","url":null,"abstract":"&lt;p&gt;In a recent study published in &lt;i&gt;Cell&lt;/i&gt;, Song et al. reported a conceptual advance by hijacking the endoplasmic reticulum–associated degradation (ERAD) pathway to enable targeted degradation of transmembrane proteins (TPs) [&lt;span&gt;1&lt;/span&gt;]. Named ERAD-engaging chimeras (ERADECs), this novel degradation strategy utilizes small molecular compounds to achieve efficient and selective degradation of TPs at low concentrations, opening a new door for the targeted protein degradation (TPD).&lt;/p&gt;&lt;p&gt;TPD is a rapidly advancing therapeutic strategy. Since the introduction of proteolysis-targeting chimeras (PROTACs) in 2001, which harness the ubiquitin–proteasome system (UPS) to selectively degrade target proteins, the field has progressed from conceptual development to clinical translation. Classical PROTAC is a heterobifunctional small molecule composed of two distinct ligands connected by a linker, one of which binds to the protein of interest (POI), whereas the other recruits and binds to E3 ligase. By simultaneously binding to both components, PROTACs induce POI ubiquitination and subsequent degradation via UPS. However, TPs are synthesized in the endoplasmic reticulum (ER) and trafficked to the plasma membrane through the vesicular system, rendering them inaccessible to the cytosolic degradation machinery. Consequently, classical PROTACs may face challenges in efficiently targeting membrane proteins, potentially limiting their therapeutic applications.&lt;/p&gt;&lt;p&gt;TPs are synthesized and folded in the ER, where stringent quality control mechanisms ensure proper protein conformation. Misfolded proteins are recognized and retrotranslocated into the cytosol via the endoplasmic reticulum–associated degradation (ERAD) pathway, where they undergo ubiquitination and subsequent proteasomal degradation. ER-resident E3 ubiquitin ligases (ER-E3s) confer substrate specificity and initiate ubiquitination [&lt;span&gt;2&lt;/span&gt;]. Building on the PROTACs paradigm, Song et al. proposed ERADECs, a conceptual framework that uses heterobifunctional chimeras to recruit ER-E3 ligases for ERAD-mediated degradation. Desonide was identified as a direct SYVN1 recruiter and was conjugated to the PD-L1 binder BMS-202 to generate P-ERADECs. These chimeras induced potent picomolar-to-nanomolar PD-L1 degradation in MDA-MB-231 and A375 cells via SYVN1-dependent ternary complex formation, ubiquitination, and proteasomal clearance (Figure 1). In vivo, systemic administration suppressed tumor growth with superior efficacy compared with atezolizumab and BMS-202. Additionally, an EGFR-targeting variant successfully reduced EGFR protein levels, confirming the utility of this strategy against diverse transmembrane protein targets. These findings establish ERADECs as a generalizable platform for degrading critical cellular targets and complement and expand the scope of PROTAC-based technologies. Notably, under physiological conditions, the ERAD pathway mediated by SYVN1 is not limited to the degrada","PeriodicalId":74135,"journal":{"name":"MedComm - Future medicine","volume":"5 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mef2.70074","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149048240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations Between Metabolic Phenotypes and Cardiovascular Outcomes in Patients Undergoing Percutaneous Coronary Intervention: A Prospective Cohort Study","authors":"Bowen Li,&nbsp;Jining He,&nbsp;Chenxi Song,&nbsp;Rui Zhang,&nbsp;Sheng Yuan,&nbsp;Zhiyong Zhao,&nbsp;Kefei Dou","doi":"10.1002/mef2.70072","DOIUrl":"https://doi.org/10.1002/mef2.70072","url":null,"abstract":"<p>Obesity and metabolic abnormalities are risk factors for cardiovascular (CV) events in patients with coronary artery disease (CAD). However, the prognostic impact of distinct metabolic phenotypes after percutaneous coronary intervention (PCI) remains unclear. We enrolled 23,882 patients undergoing PCI at Fuwai Hospital between 2017 and 2018. Obesity was defined as body mass index (BMI) ≥ 28.0 kg/m², and metabolic unhealth was defined as diabetes or hypertension plus dyslipidemia. Patients were classified into four phenotypes: metabolically healthy non-obese (MHN), metabolically healthy obese (MHO), metabolically unhealthy non-obese (MUN), and metabolically unhealthy obese (MUO). Primary endpoint was 3-year CV events, including CV death, non-fatal MI, and non-fatal stroke. During a median follow-up of 36 months, 757 (3.2%) CV events occurred. Compared with MHN, MUN was associated with higher CV risk (HR 1.27, 95% CI 1.07–1.52). The excess risk in MUN was mainly driven by non-fatal MI (HR 1.47, 95% CI 1.09–1.99) and stroke (HR 1.71, 95% CI 1.07–2.75). Among metabolically unhealthy patients, non-obese individuals had higher all-cause mortality than obese individuals (HR 1.50, 95% CI 1.12–2.02). Metabolically unhealthy non-obese patients had increased CV risk after PCI. Metabolic phenotype stratification may improve risk prediction in CAD patients.</p>","PeriodicalId":74135,"journal":{"name":"MedComm - Future medicine","volume":"5 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mef2.70072","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149047960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isocitrate Dehydrogenase (IDH) Mutations in Hematological Malignancies: Epidemiology, Mechanisms, and Therapeutic Strategies","authors":"Jinkun Xu,&nbsp;Haiying Bai,&nbsp;Lijuan Hu","doi":"10.1002/mef2.70070","DOIUrl":"https://doi.org/10.1002/mef2.70070","url":null,"abstract":"<p>Isocitrate dehydrogenase (IDH) mutation is an important molecular abnormality in hematological malignancies, occurring widely in various disease types such as acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), and myelodysplastic syndrome (MDS). IDH mutations promote the occurrence and progression of hematological tumors through mechanisms such as epigenetic modification, affecting metabolism and the immune microenvironment. The prognostic significance of IDH mutations highly depends on factors such as disease subtype and mutation site, presenting complex clinical heterogeneity. However, the optimal application strategy of IDH inhibitors in combination therapy and the systematic response plan for drug resistance mechanisms are still lacking a unified consensus at present. This article systematically reviews the incidence and prognosis of IDH mutations in hematological tumors, the carcinogenic mechanism of IDH mutations, and the drug resistance mechanism of IDH inhibitors. It also discusses the clinical efficacy, safety, and combination therapy strategies of the marketed IDH inhibitors (Ivosidenib and Olutasidenib for IDH1 mutations, and Enasidenib for IDH2 mutations). Moreover, emerging technologies are introduced. This review systematically integrates the basic mechanisms of IDH mutations to the clinical translation of related research progress, aiming to provide theoretical and reference basis for clinical treatment decisions and subsequent basic research.</p>","PeriodicalId":74135,"journal":{"name":"MedComm - Future medicine","volume":"5 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mef2.70070","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149047959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Scavenger Receptor Class F Member 2: An Intracellular Receptor Escorting Hepatitis B Virus From Endosome to Nuclear Pore","authors":"Yujing Ng,&nbsp;Lin Du,&nbsp;Huahao Fan","doi":"10.1002/mef2.70071","DOIUrl":"https://doi.org/10.1002/mef2.70071","url":null,"abstract":"&lt;p&gt;In a recent study published in &lt;i&gt;Cell&lt;/i&gt;, Li et al. identified scavenger receptor class F member 2 (SCARF2) as an intracellular receptor for hepatitis B virus (HBV) that facilitates viral nucleocapsid transport from endosomal vesicles to the nuclear pore complex (NPC), revealing a previously unrecognized mechanism underlying HBV cytoplasmic-to-nuclear trafficking. This finding provides new insight into the mechanisms governing HBV entry and intracellular trafficking [&lt;span&gt;1&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;HBV infection remains a major global health burden, impacting approximately 296 million individuals worldwide [&lt;span&gt;2&lt;/span&gt;]. Although nucleos(t)ide analogs effectively suppress viral replication, they rarely achieve a functional cure because covalently closed circular DNA (cccDNA) persists in the nucleus [&lt;span&gt;3&lt;/span&gt;]. The entry of HBV into host hepatocytes involves a complex multistep process. Initially, the S domain of the virus engages in a low-affinity attachment to heparan sulfate proteoglycans (HSPGs), followed by high-affinity binding of the preS1 region of the large envelope protein to the cell-surface receptor sodium taurocholate co-transporting polypeptide (NTCP), the functional entry receptor for HBV and hepatitis D virus (HDV) [&lt;span&gt;4&lt;/span&gt;]. Nevertheless, the subsequent intracellular trafficking of the internalized virion to the nuclear periphery has remained incompletely understood.&lt;/p&gt;&lt;p&gt;To elucidate the host factors acting after HBV engages with NTCP, Li et al. screened 74 membrane proteins with liver-enriched expression in HepG2-NTCP cells, defined as at least fivefold higher mRNA expression in the liver than in other tissues. Their findings revealed that CREBH (cyclic AMP-responsive element-binding protein H; encoded by CREB3L3) emerged as a prominent hit, with its overexpression increasing HBV infection by 2–4-fold, whereas its knockdown reduced infection. CREBH is an endoplasmic-reticulum membrane-bound transcription factor with important roles in hepatic metabolic and stress-responsive gene regulation. Through the construction of truncated CREBH mutants, the authors further demonstrated that its transcriptional activation function was essential for its pro-infectious activity, suggesting that CREBH promotes HBV infection through downstream transcriptional regulation. To identify potential target genes, whole-transcriptome sequencing revealed 321 genes upregulated following CREBH overexpression and 1593 genes downregulated following CREBH knockdown. Intersection analysis identified 62 genes co-regulated by CREBH, among which only &lt;i&gt;SCARF2&lt;/i&gt; reproduced the infection-promoting effect of CREBH when individually overexpressed (Figure 1A). Unlike CREBH, which acts through transcriptional regulation, SCARF2 functions at a post-translational, intracellular stage of infection. Thus, the CREBH-to-SCARF2 axis provides a plausible link between a liver-enriched transcriptional program and HBV entry. Importantly, silencing SCARF2 in HepG2","PeriodicalId":74135,"journal":{"name":"MedComm - Future medicine","volume":"5 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mef2.70071","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148993998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial Transfer From Satellite Glial Cells to Neurons via Tunneling Nanotubes: A New Protective Axis for Peripheral Neuropathy","authors":"Qing Ye,&nbsp;Jialuoyang Chen,&nbsp;Guihua Wei","doi":"10.1002/mef2.70069","DOIUrl":"https://doi.org/10.1002/mef2.70069","url":null,"abstract":"&lt;p&gt;In a recent study published in Nature, Xu et al. reported that Satellite glial cells (SGCs) in the dorsal root ganglia (DRG) transfer mitochondria to primary sensory neurons via &lt;i&gt;MYO10&lt;/i&gt;-dependent tunneling nanotubes (TNTs) [&lt;span&gt;1&lt;/span&gt;]. This discovery establishes the key neuro-glial mitochondrial supply and demonstrates that mitochondrial or glial transplantation offers a new therapeutic strategy against neuropathic pain.&lt;/p&gt;&lt;p&gt;Neuropathic pain (NP) has been officially defined as “pain caused by a lesion or disease of the somatosensory system”. Over the past decades, the number of clinical research devoted to neuropathic pain has dramatically increased. Among them, Patients with painful neuropathies (diabetic or non-diabetic), often showed burning, cold pain, electric shocks, tingling, pins and needles, numbness, and itch. Furthermore, up to 70% of people exposed to neurotoxic chemotherapy, such as oxaliplatin or cisplatin, may have acute chemotherapy-induced peripheral neuropathy (CIPN) [&lt;span&gt;2&lt;/span&gt;]. Emerging evidence indicates that NP is fundamentally driven by an intricate neuro-metabolic failure within DRG. The inability of primary sensory neurons to meet their exceptionally high mitochondrial demands are recognized as a hallmark of nerve regeneration. Understanding the neural microenvironment, particularly the homeostatic interactions between neurons and their surrounding SGCs, may be the effective therapeutic strategy for NP.&lt;/p&gt;&lt;p&gt;Unlike neurons in the central nervous system, the primary sensory neurons in the DRG are the pseudounipolar cells, whose axons extend up to 100 cm to connect the peripheral organs with the spinal cord [&lt;span&gt;3&lt;/span&gt;]. This expansive axonal structure creates large challenges for mitochondrial transport and energy distribution from the cell body to distal terminals [&lt;span&gt;4&lt;/span&gt;]. To overcome these bioenergetic constraints, SGCs, which uniquely and tightly envelope neuronal cell bodies within the DRG, maintain an external mitochondrial “supply chain” to support neuronal metabolic homeostasis. Using scanning and transmission electron microscopy (SEM/TEM), Xu et al. successfully resolved that tunneling-nanotube-like structures (TNT-LS) play an important role in connecting SGCs to neurons in both mouse and human DRG tissue. This supply chain consists of the tripartite system: (1) The structural formation of TNTs propelled by the molecular motor &lt;i&gt;MYO10&lt;/i&gt;; (2) Neuronal endocytosis and subsequent internalization of glial-derived mitochondria; (3) The stabilization of these intercellular bridges via Connexin 43-mediated gap communication.&lt;/p&gt;&lt;p&gt;Structurally, this mitochondrial conduit relies on elastic, F-actin-based TNTs. These structures are propelled by the unconventional molecular motor &lt;i&gt;MYO10&lt;/i&gt;. Single-nucleus RNA sequencing (&lt;i&gt;snRNA-seq&lt;/i&gt;) reveals a sharp expression contrast: SGCs represent the most abundant cell population in human DRG (31.1%), yet they harbor nearly all &lt;i&gt;MYO10&lt;/i&gt; t","PeriodicalId":74135,"journal":{"name":"MedComm - Future medicine","volume":"5 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mef2.70069","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148848792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “Research Progress on Application of Dental Stem Cells in Alveolar Bone and Periodontal Regeneration”","authors":"","doi":"10.1002/mef2.70068","DOIUrl":"https://doi.org/10.1002/mef2.70068","url":null,"abstract":"<p>Z. Liu, C. Guo, J. Guo, S. Huang, and P. Du, “Research Progress on Application of Dental Stem Cells in Alveolar Bone and Periodontal Regeneration,” <i>MedComm – Future Medicine</i> 3 (2024): e98. doi:10.1002/mef2.98</p><p>Following publication of the Review Article, the authors identified an error in the reference list. Reference 150 was cited in support of the statement that hydrogels “mimic natural tissue properties and create unique microenvironments for cellular signals during stem cell differentiation.” The original reference (Sahab Negah S, et al., <i>Cell Mol Neurobiol</i>. 2020;40[3]:283–299) discusses neurogenic signaling microenvironments but does not address hydrogels as biomaterial scaffolds, and was therefore not optimally suited to the context.</p><p>The authors have corrected this error by replacing reference 150 with the following:</p><p>150. N. Huebsch, E. Lippens, K. Lee, et al., “Matrix Elasticity of Void-Forming Hydrogels Controls Transplanted-Stem-Cell-Mediated Bone Formation,” <i>Nature Materials</i> 14, no. 12 (2015): 1269–1277.</p><p>This correction does not affect the conclusions of the manuscript. The authors apologize for this error and any confusion it may have caused.</p><p>We apologize for this error.</p>","PeriodicalId":74135,"journal":{"name":"MedComm - Future medicine","volume":"5 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mef2.70068","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “Recent Advances of Transformers in Medical Image Analysis: A Comprehensive Review”","authors":"","doi":"10.1002/mef2.70066","DOIUrl":"https://doi.org/10.1002/mef2.70066","url":null,"abstract":"<p>K. Xia and J. Wang, “Recent Advances of Transformers in Medical Image Analysis: A Comprehensive Review,” <i>MedComm – Future Medicine</i> 2 (2023): e38. https://doi.org/10.1002/mef2.38</p><p>In the version of this Review Article originally published, the reference list contained a duplicate reference: Reference 124 was a duplicate of Reference 128. The duplicate reference (Reference 124) should be removed.</p><p>As a result of this correction, the entries in the first column of Table 2 corresponding to the original rows 46 (“Zhang”) and 50 (“MIA-COV19D”) have been merged into a single entry, which now reads “Zhang &amp; Wen.”</p><p>We apologize for this error.</p>","PeriodicalId":74135,"journal":{"name":"MedComm - Future medicine","volume":"5 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mef2.70066","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “Stem Cell-Derived Exosomes as Nanotherapeutics for Inflammatory Diseases”","authors":"","doi":"10.1002/mef2.70067","DOIUrl":"https://doi.org/10.1002/mef2.70067","url":null,"abstract":"<p>Wei, X., Wang, Q., Wen, W., Yang, L., Chen, H., Xu, G., Zhou, Y., Yang, J. and Duan, Z. (2025), Stem Cell-Derived Exosomes as Nanotherapeutics for Inflammatory Diseases. MedComm – Future Medicine, 4: e70016. https://doi.org/10.1002/mef2.70016</p><p>In paragraph 2 of the “Introduction” section, the text “There is growing evidence that SCs can secrete extracellular vehicles (EVs) with lipid bilayer structures, including exosomes (Exos), microvesicles and apoptotic bodies.” was incorrect. This should have read: “There is growing evidence that SCs can secrete extracellular vesicles (EVs) with lipid bilayer structures, including exosomes (Exos), microvesicles and apoptotic bodies.”</p><p>In paragraph 4 of the “Separation, Characterization and Engineering of SC-Exos” section, the text “Taking MSC-Exos as an example, currently, they can be isolated from SC culture super nuances by ultrafast centrifugation, polymerization precipitation, density gradient centrifugation, column chromatography, and immune magnetic beads.” was incorrect. This should have read: “Taking MSC-Exos as an example, currently, they can be isolated from SC culture supernatants by ultrafast centrifugation, polymerization precipitation, density gradient centrifugation, column chromatography, and immune magnetic beads.”</p><p>We apologize for these errors.</p>","PeriodicalId":74135,"journal":{"name":"MedComm - Future medicine","volume":"5 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mef2.70067","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}