AIMS/BACKGROUND:Urticaria is a common inflammatory skin disease that significantly impairs the quality of life and mental health of adolescents and young adults. Despite its increasing impact, comprehensive long-term epidemiological data focusing specifically on the young population across diverse Asian regions remain limited. This study aimed to assess the burden of urticaria among adolescents and young adults in Asia from 1990 to 2021, and to project its changes through 2036. METHODS:A repeated cross-sectional analysis using Global Burden of Disease (GBD) Study 2021 data was conducted to estimate the burden of urticaria prevalence, incidence, and disability-adjusted life years (DALYs) among Asian adolescents and young adults (ages 10-24) from 1990 to 2021. Data analysis was performed from November 2024 to April 2025. RESULTS:From 1990 to 2021, the prevalence, incidence, and DALYs for urticaria increased among Asian adolescents and young adults, with rates consistently higher in females. In 2021, there were 16,347,995 new cases (95% uncertainty interval [UI]: 12,625,370 to 21,681,388). The prevalence rose from 863.13 (95% UI: 761.99 to 983.08) to 877.84 (95% UI: 775.68 to 1000.20) per 100,000 population (average annual percent change [AAPC] = 0.055%, 95% confidence interval [CI]: 0.053% to 0.056%). The incidence increased from 1525.51 (95% UI: 1341.63 to 1728.55) to 1552.60 (95% UI: 1369.05 to 1758.22) per 100,000 population (AAPC = 0.057%, 95% CI: 0.055% to 0.057%). The DALY rate grew from 51.74 (95% UI: 34.15 to 74.31) to 52.78 (95% UI: 34.65 to 76.09) per 100,000 population (AAPC = 0.064%, 95% CI: 0.063% to 0.065%). Overall, Central Asia has the highest age-standardized prevalence, incidence, and DALYs. Health inequality assessments indicated that the disease burden has intensified in low socio-demographic index (SDI) regions due to unequal medical resources. The incidence is projected to continue rising over the next 15 years, reaching 1568.89 (95% prediction interval [PI]: 1552.24 to 1592.05) per 100,000 population by 2036. CONCLUSION:Over the past three decades, urticaria has shown significant increases in prevalence, incidence, and DALYs across the region, with females exhibiting higher morbidity rates than males. This trend is expected to persist through 2036. These findings underscore the urgent need for targeted public health interventions and more equitable distribution of medical resources to mitigate the escalating disease burden, particularly in high-burden, low-SDI regions.

GCMN is a major risk factor for melanoma in children, which occurs sporadically, but familial cases are rarely reported. WGS results revealed the presence of a G3BP1-BRAF fusion in tumor tissue in our case. We hope that this case provides some reference for the diagnosis, prognosis, and individualized treatment of newborn patients with GCMN.

MicroRNAs (miRs) are a class of non-coding RNA molecules that regulate gene expression post-transcriptionally. MiRs, as translational repression and/or degradation of target messenger RNAs, are critical regulators of various physiological processes, including cell proliferation, differentiation, death, and immune responses. Currently, miRs are being investigated as potential biomarkers and therapeutic targets for a range of diseases. In recent years, miRs have been reported to be implicated in several pathophysiological processes of dermatological diseases including psoriasis, skin wound, diabetic skin wound, burn, systemic sclerosis, skin tumors (melanoma, squamous cell carcinoma and basal cell carcinoma), recessive dystrophic epidermolysis bullosa, and systemic lupus erythematosus. Mechanistically, the regulation of oxidative stress, inflammation, apoptosis, and angiogenesis may account for the distinct roles of miRs in the skin. A deeper understanding of different miRs and their related regulatory targets is essential for elucidating the pathophysiology of numerous skin diseases. This review briefly summarizes roles and potential applications of miRs within the skin. The combination of miRs with novel materials or compounds may offer innovative approaches for the treatment of skin diseases. However, further research is necessary to facilitate the translation into clinical applications for dermatological diseases.

Resistance to cell death is one of the core hallmarks of cancer, with regulatory abnormalities particularly pronounced in the malignant progression and therapeutic resistance of melanoma. This review aims to systematically summarize the roles and mechanisms of regulated cell death (RCD) in melanoma. Currently, distinct types of RCD, including apoptosis, autophagy, pyroptosis, immunogenic cell death, necroptosis, and ferroptosis, have all been found to be involved in melanoma. Autophagy promotes the survival of melanoma cells under stress conditions through metabolic adaptation, yet its excessive activation can trigger cell death. Immunogenic cell death has the capacity to elicit adaptive immune responses in immunocompetent syngeneic hosts. Necroptosis, governed by the receptor-interacting protein kinase 1 (RIPK1)/RIPK3 mixed lineage kinase domain-like protein (MLKL) signaling axis, can synergize with immunotherapy to enhance anti-melanoma immune responses when activated. Pyroptosis, mediated by Gasdermin proteins, induces the release of inflammatory factors that reshape the tumor microenvironment and enhance the efficacy of immune checkpoint inhibitors. Ferroptosis, characterized by lipid peroxidation, can overcome melanoma resistance by targeting the solute carrier family 7 member 11 (SLC7A11)/glutathione peroxidase 4 (GPX4) axis. Therapeutic strategies targeting RCD pathways have demonstrated breakthrough potential. Several agents have been developed to target RCD in order to suppress melanoma.

Regulated cell death like pyroptosis is one vital cause of diabetic cardiomyopathy (DCM), which eventually leads to heart failure. Tumor necrosis factor (TNF) receptor-associated death domain protein (TRADD) is an adapter protein with multiple functions that participates in the pathophysiological progress of different cardiovascular disorders via regulating regulated cell death. Studies have shown that TRADD combines with receptor-interacting protein kinase 3 (RIPK3) and facilitates its activation, thereby mediating TNF-induced necroptosis. However, no direct relationship between TRADD and pyroptosis has been identified. In this study, we investigated the role and mechanisms of TRADD in pyroptosis during DCM. We established a streptozotocin (STZ)-induced diabetic mouse model and high glucose (HG)-treated cardiomyocytes model. We showed that the expression levels of TRADD were significantly increased in the hearts of diabetic mice and HG-treated cardiomyocytes. Knockdown of TRADD did not affect blood glucose and triglyceride levels, but significantly improved cardiac function, and attenuated myocardial hypertrophy, fibrosis, and pyroptosis in the heart of diabetic mice. Furthermore, both knockdown of TRADD and application of TRADD inhibitor apostatin-1 (Apt-1, 10 μM) significantly ameliorated cell injury and pyroptosis in HG-treated cardiomyocytes. We demonstrated that HG treatment increased the expression of X-box binding protein 1 (XBP1) and enhanced the binding of XBP1 to the TRADD promoter to elevate TRADD expression in the cardiomyocytes. Collectively, this study provides evidence that TRADD-mediated pyroptosis contributes to DCM, suggesting that strategies to inhibit TRADD activity may be a novel approach for DCM treatment.

Hydrogen sulfide (H2S), recognized as the third gasotransmitter, plays a pivotal role in the pathophysiological processes of various diseases. Cystathionine γ-lyase (CSE) is the main enzyme for H2S production in the skin. However, effects and mechanisms of H2S in diabetic skin wound healing remain unclear. Our findings revealed a decrease in plasma H2S content in diabetic patients with skin wounds. CSE knockout (KO) diabetic mice resulted in delayed wound healing, reduced blood perfusion, and CD31 expression around the wounds. It also led to increased infiltration of inflammatory cells and M1-type macrophages, decreased collagen levels, α-smooth muscle actin (α-SMA), and proliferating cell nuclear antigen (PCNA) expression. Additionally, there were enhanced expressions of necroptosis related proteins, including receptor interacting protein kinase 1 (RIPK1), RIPK3 and mixed lineage kinase domain like protein (MLKL). In comparison, sodium hydrosulfide (NaHS), H2S donor, accelerated skin wound healing in leptin receptor deficiency (db/db) mice. This acceleration was accompanied by increased blood perfusion and CD31 expression, reduced infiltration of inflammatory cells and M1-type macrophages, elevated collagen levels, α-SMA, and PCNA expressions, and decreased necroptosis-related protein expressions together with nuclear factor-κB (NF-κB) p65 phosphorylation. In conclusion, H2S regulates macrophage polarization and necroptosis, contributing to the acceleration of diabetic skin wound healing. These findings offer a novel strategy for the treatment of diabetic skin wounds.

Proline rich protein 14 (PRR14) is considered as a new component of the nuclear fiber layer, it may be a key molecule in mediating nuclear morphological changes and functional changes in tumorigenesis. But, it's still unclear in human cutaneous squamous cell carcinoma (cSCC). In the study, the expression profiles of PRR14 in patients with cSCC were investigated by immunohistochemistry (IHC), also the PRR14 expression in cSCC tissues were detected using the methods of real-time quantitative PCR (RT-qPCR) and Western blot; cell counting kit-8 (CCK-8) assay, wound healing assay, matrigel-based transwell assay and Annexin V-FITC and PI double-staining with flow cytometry assay were used to investigate the biological functions of PRR14 in A431 and HSC-1 cSCC cells. Overexpression of PRR14 in cSCC patients was reported firstly in this study and its high expression was related to differentiation, thickness and tumor node metastasis (TNM) stage of cSCC. PRR14 inhibition with RNA interfering (RNAi) method resulted in the suppression of cell proliferation, migration and invasion but promotion the apoptosis of cSCC cells, and upregulation of the protein phosphorylation levels of mammalian target of rapamycin (mTOR), phosphoinositide 3-kinase (PI3K) and Akt. The study shows PRR14 maybe an activator of cSCC carcinogenesis through PI3K/Akt/mTOR signal pathway, and it also maybe a prognostic factor and new therapeutical target for cSCC treatment.

N6-Methyladenosine (m6A) is the most common mRNA modification in eukaryotes and is a dynamically reversible posttranscriptional modification. The enzymes involved in m6A modification mainly include methyltransferases (writers), demethylases (erasers), and methylated readers (Readers). m6A modification is mainly catalyzed by m6A methyltransferase and removed by m6A demethylase. The modified RNA can be specifically recognized and bound by m6A recognition protein. This protein complex then mediates RNA splicing, maturation, nucleation, degradation, and translation. m6A also alters gene expression and regulates cellular processes such as self-renewal, differentiation, invasion, and apoptosis. An increasing body of evidence indicates that the m6A methylation modification process is closely related to the occurrence of various skin diseases. In this review, we discuss the role of m6A methylation in skin development and skin diseases including psoriasis, melanoma, and cutaneous squamous cell carcinoma.

An excessive proliferation of skin fibroblasts usually results in different skin fibrotic diseases. Hydrogen sulphide (H2 S) is regarded as an important endogenous gasotransmitter with various functions. The study aimed to investigate the roles and mechanisms of H2 S on primary mice skin fibroblasts proliferation. Cell proliferation and collagen synthesis were assessed with the expression of α-smooth muscle actin (α-SMA), proliferating cell nuclear antigen (PCNA), Collagen I and Collagen III. The degree of oxidative stress was evaluated by dihydroethidium (DHE) and MitoSOX staining. Mitochondrial membrane potential (ΔΨm) was detected by JC-1 staining. Necroptosis was evaluated with TDT-mediated dUTP nick end labelling (TUNEL) and expression of receptor-interacting protein kinase 1 (RIPK1), RIPK3 and mixed lineage kinase domain-like protein (MLKL). The present study found that α-SMA, PCNA, Collagen I and Collagen III expression were increased, oxidative stress was promoted, ΔΨm was impaired and positive rate of TUNEL staining, RIPK1 and RIPK3 expression as well as MLKL phosphorylation were all enhanced in skin fibroblasts from cystathionine γ-lyase (CSE) knockout (KO) mice or transforming growth factor-β1 (TGF-β1, 10 ng/mL)-stimulated mice skin fibroblasts, which was restored by exogenous sodium hydrosulphide (NaHS, 50 μmol/L). In conclusion, endogenous H2 S production impairment in CSE-deficient mice accelerated skin fibroblasts proliferation via promoted necroptosis, which was attenuated by exogenous H2 S. Exogenous H2 S supplement alleviated proliferation of skin fibroblasts with TGF-β1 stimulation via necroptosis inhibition. This study provides evidence for H2 S as a candidate agent to prevent and treat skin fibrotic diseases.

Background: The purpose of the current research was to investigate the biological roles of LINC00467 in inducing melanoma deterioration. Methods: Differential level of LINC00467 in melanoma tissues and its prognostic value were analyzed in GEPIA, which were further confirmed in clinical samples we collected. Regulatory effects of LINC00467 on proliferation, migration and invasion capacities of A375 and SKMEL1 cell lines were examined by a series of functional experiments. Potential downstream targets of LINC00467 were identified through dual-luciferase reporter assay, and their synergistic role in melanoma process was finally explored by rescue experiments. Results: LINC00467 was up-regulated in melanoma samples, but it did not have a prognostic potential in melanoma. LINC00467 has the capacities to stimulate proliferation, migration and invasion of A375 and SKMEL1 cell lines. The feedback loop LINC00467/miR-485-5p/PAK1 was identified, which was responsible for inducing melanoma deterioration. Conclusions: LINC00467 stimulates proliferation, migration and invasion capacities of melanoma via targeting miR-485-5p to upregulate PAK1, which provides potential targets for treatment of melanoma.

目的 探讨序贯外用0.05％地奈德乳膏与2％克立硼罗软膏治疗轻中度特应性皮炎(atopic dermatitis,AD)的疗效、安全性及复发率.方法 选取2021年7月至2022年8月南通大学附属医院皮肤科门诊轻至中度AD患者179例,随机分为3组:序贯治疗组外用0.05％地奈德乳膏连续治疗2周后,换用2％克立硼罗软膏,继续治疗2周;地奈德组外用0.05％地奈德乳膏连续治疗2周,接着每周2次再治疗2周;克立硼罗组外用2％克立硼罗软膏连续治疗4周.比较3组患者治疗前后的特应性皮炎评分(scoring atopic dermatitis,SCORAD)、治疗后的临床疗效、不良反应发生率及随访停药4周后的复发率.结果 序贯治疗组治疗后的SCORAD评分为(6.69±6.31)分、有效率为82.5％,与地奈德组[(5.39±4.25)分,87.5％]比较,差异无统计学意义;与克立硼罗组[(11.25±8.82)分,54.7％]比较,差异有统计学意义(P=0.002).序贯治疗组、地奈德组和克立硼罗组患者的复发率和不良反应发生率分别为12.8％、31.0％、13.8％和8.8％、22.9％、9.4％,组间差异均无统计学意义.结论 序贯外用0.05％地奈德乳膏与2％克立硼罗软膏治疗轻中度AD,临床疗效较好、安全性良好、复发率低,值得临床推广应用.

Keloid is a common dermatofibrotic disease with excessive skin fibroblast proliferation. Hydrogen sulfide (H2S) as the third gasotransmitter improves fibrosis of various organs and tissues. Our study is aimed at investigating the effects and possible mechanisms of H2S on skin fibroblast proliferation. Scar tissues from six patients with keloid and discarded skin tissue from six normal control patients were collected after surgery, respectively. Plasma H2S content and skin H2S production in patients with keloid were measured. Keloid fibroblasts and transforming growth factor-β 1- (TGF-β 1, 10 ng/mL) stimulated normal skin fibroblasts were pretreated with H2S donor as NaHS (50 μM) for 4 h. Cell migration after scratch was assessed. The expressions of α-smooth muscle actin (α-SMA), proliferating cell nuclear antigen (PCNA), collagen I, and collagen III were detected by immunofluorescence, real-time PCR, and/or Western blot. Intracellular superoxide anion and mitochondrial superoxide were evaluated by dihydroethidium (DHE) and MitoSOX staining, respectively. Mitochondrial membrane potential was detected by JC-1 staining. Apoptotic cells were detected by TDT-mediated dUTP nick end labeling (TUNEL). The expressions of receptor interacting protein kinase 1 (RIPK1), RIPK3, and mixed lineage kinase domain-like protein (MLKL) were measured by Western blot. We found that H2S production was impaired in both the plasma and skin of patients with keloid. In keloid fibroblasts and TGF-β 1-stimulated normal skin fibroblasts, exogenous H2S supplementation suppressed the expressions of α-SMA, PCNA, collagen I, and collagen III, reduced intracellular superoxide anion and mitochondrial superoxide, improved the mitochondrial membrane potential, decreased the positive rate of TUNEL staining, and inhibited RIPK1 and RIPK3 expression as well as MLKL phosphorylation. Overall, H2S suppressed skin fibroblast proliferation via oxidative stress alleviation and necroptosis inhibition.

目的:分析二氧化碳激光联合光动力治疗外阴尖锐湿疣的临床疗效和不良反应情况.方法:回顾分析2019年1月—2020年1月在南通大学附属医院皮肤科治疗的外阴尖锐湿疣患者160例,按治疗方法不同分为两组,每组80例.对照组采用二氧化碳激光治疗,观察组采用二氧化碳激光联合光动力治疗,统计3个月后的疗效及6个月后的复发率.结果:治疗3个月后,观察组的有效率为93.75％,对照组为70.00％(P<0.05).6个月后随访观察组的复发率(6.25％)明显低于对照组(26.25％)(P<0.05),观察组疼痛评分显著低于对照组,不良反应消退时间及创面愈合时间均短于对照组(均P<0.05).结论:二氧化碳激光联合光动力治疗外阴尖锐湿疣临床效果显著,能明显改善临床复发率,缓解患者疼痛,加速患者创面愈合,值得临床推广应用.

Hedgehog (Hh) signaling has been proved to be closely associated with the occurrence of melanoma. Wogonin is one of the active components of flavonoids that extracts from Scutellariae radix. Previous studies showed that wogonin could inhibit the invasion and migration of B16F10 cells, and suppress the synthesis of melanin in A375 melanoma cells. However, the regulatory effects of Hh signaling in wogonin against melanoma and its potential mechanisms remain largely unknown. The present study aimed to investigate the effect of wogonin on the growth of HT144 melanoma, and to elucidate the role of Hh signaling in wogonin-induced antitumor effects by focusing on inflammation and glycolysis regulation. Wogonin inhibited the proliferation, colony formation and tumor growth of HT144 melanoma cells. Wogonin showed strong anti-inflammatory effect in HT144 melanoma, as shown by the decreased levels of pro-inflammatory factors, the increased level of anti-inflammatory factor and the decreased expression of inflammatory cytokines. Wogonin decreased the glucose consumption and the production of lactic acid and ATP, and decreased the activities of hexokinase (HK), phosphofructokinase (PFK) and pyruvate kinase (PK), and further inhibited the expression of monocarboxylate transporter 1 (MCT-1), MCT-4 and glucose cotransporter-1 (GLUT1), showing potent anti-glycolysis effect against HT144 melanoma. Wogonin inhibited the patched and Smo expression while increased Hhip expression in HT144 cells, suggesting that wogonin blocked the Hh signaling in HT144 cells. The Hh signaling inhibitor cyclopamine, like wogonin, inhibited the colony formation of HT144 cells, however, the inhibitory effect of wogonin on colony formation of HT144 cells was abrogated by the Hh signaling agonist SAG. In addition, SAG abrogated the inhibitory effect of wogonin on the secretion of inflammatory factors and the expression of inflammatory cytokines. Furthermore, SAG abrogated the inhibitory effect of wogonin on several key molecules controlling glycolysis. Overall, these findings suggested that the anti-tumor effect of wogonin can be attributed to the inhibition of Hh signaling-mediated regulation of inflammation and glycolysis in HT144 melanoma.

Background: Hydrogen sulfide (H2S) is now recognized as a vital endogenous gasotransmitter with a variety of biological functions in different systems. Recently, studies have increasingly focused on the role of H2S in the skin. Aim of Review: This review summarizes recent progress and provides perspectives on H2S in the treatment of dermatological diseases. Key Scientific Concepts of Review: Three H2S production enzymes, cystathionine-γ-lyase (CSE), cystathionine-β-synthase (CBS) and 3-mercaptopyruvate sulfur transferase (3-MST), are all present in the skin, and it is likely that different cell types in the skin express them differently. Previous studies have demonstrated that H2S protects against several dermatological diseases, such as burns, diabetic skin wounds, psoriasis, skin flap transplantation, systemic sclerosis, melanoma, and pruritus. The mechanism might be related to the regulation of oxidative stress, inflammation, angiogenesis, apoptosis, and allergic reactions. H2S-based therapeutics require certain characteristics for topical delivery, for example, controlled release, appropriate physicochemical properties, good storage stability, acceptable odor, and advanced delivery systems. H2S-induced S-sulfhydration on proteins are potential novel targets for therapeutic intervention and drug design for the skin, which may lead to the development and application of H2S-related drugs for dermatological diseases.

摘要： 患者男，26岁，左面部皮下包块1年于2019年5月9日至宿迁市第一人民医院皮肤科就诊。1年前患者触及左面部有一黄豆大小皮下包块，生长缓慢，随气温变化其大小略有改变。既往体健，无结节性硬化症、神经纤维瘤病家族史……

目的:总结葡萄球菌性烫伤样皮肤综合征(staphylococcal scalded skin syndrome,SSSS)的临床特点.方法:回顾性分析2012年1月—2019年7月住院的31例SSSS患儿的临床表现、伴随症状、实验室检查、治疗方法及转归.结果:31例SSSS患儿中≤4岁占64.5％,入院前误诊为其他疾病9例(27.3％),发病前有明显诱因13例.31例均予抗生素治疗,其中同时予小剂量地塞米松21例,同时予小剂量地塞米松和静脉注射免疫球蛋白(intravenous immunoglobulin,IVIG)5例.所有患儿均痊愈出院,住院时间4～10 d,平均(6.30±1.60)d.3组SSSS患儿皮肤触痛消失时间、皮疹控制时间比较差异均无统计学意义(均P>0.05),住院时间比较差异有统计学意义(P<0.05).结论:早期有效抗生素联合小剂量地塞米松治疗SSSS效果显著,同时联合IVIG治疗可快速有效地控制症状.

The obligate intracellular bacterium Chlamydia trachomatis is a group of worldwide human pathogens that can lead to serious reproductive problems. The frequent clinical treatment failure promoted the development of novel antichlamydial agents. Here, we firstly reported a group of pyrroloisoxazolidine-inhibited C. trachomatis in a dose-dependent manner in vitro. Among them, compounds 1 and 2 exhibited the strongest inhibitory activity with IC50 values from 7.25 to 9.73 μM. The compounds disturbed the whole intracellular life cycle of C. trachomatis, mainly targeting the middle reticulate body proliferation stages. Besides, the compounds partially inhibited the chlamydial infection by reducing elementary body infectivity at high concentration. Our findings suggest the potential of pyrroloisoxazolidine derivatives as promising lead molecules for the development of antichlamydial agents.

BACKGROUND:In the past century, many phenazines were isolated from the marine microorganism, and some of these phenazines possessed potent antibacterial activities. We found that a few of the synthesized 4-substituted phenazines could block the infectivity of chlamydiae without host cell toxicity.OBJECTIVE:The aim of this study was to design and synthesize two series of novel 3-substituted phenazines to find novel antichlamydial agents.METHODS:The 3-substituted phenazines were synthesized via Buchwald-Hartwig cross coupling reaction and Suzuki reaction from 3-bromo-1-methoxyphenazine. The antichlamydial activity of these synthesized compounds was evaluated by determining their effect on the yield of infectious progeny EBs. Cytotoxicity of these compounds on host cells was assessed by the treatment of uninfected HeLa cells using WST-1 method.RESULTS:Most of the 3-substituted phenazines possessed potent antichlamydial activity with IC50 values from 0.15 to 12.08 μM against Chlamydia trachomatis L2, C. muridarum MoPn and C. pneumoniae AR39. Among them, 7d and 9a exhibited better antichlamydial activity with IC50 values from 0.20 to 1.01 μM while they have no apparent cytotoxicity to host cells. Biological assay disclosed that both 7d and 9a inhibited chlamydial infection by reducing elementary body infectivity and disturbing chlamydial growth during the whole chlamydial developmental cycle.CONCLUSION:Our findings suggested that 3-substituted phenazine derivatives might be a promising class of therapeutic agents for chlamydial infections. More effective phenazines with low toxicity could be acquired through further chemical modification on C-3 position rather than C-4 position of phenazine.

Chemodynamic therapy (CDT) has aroused extensive attention for cancer treatment in the last five years, as it could suppress tumor progression through in situ detrimental oxidative stress of the tumor cells via the Fenton reaction. Under a tumor acidic microenvironment, the Fenton reaction can be initiated for disproportioning endogenous hydrogen peroxide into highly toxic hydroxyl radical. Taking advantage of the highly tumor-specific therapy modality, various Fenton nanocatalysts have been developed for CDT. In particular, iron-containing Fenton nanocatalysts with minimal cytotoxicity exhibit great promise for clinical translation. In this review, we summarize the recent progress of CDT based on iron-containing nanomaterials, including iron oxide nanoparticles, glassy iron nanoclusters, ferrocene nanoparticles, metal polyphenol networks, metal-organic frameworks, etc. We also discuss the challenges and perspectives for promoting CDT by rational design of iron-containing nanomaterials, highlighting their potential for precise cancer therapy.