High-Throughput Growth of Armored Perovskite Single Crystal Fibers for Pixelated Arrays.

The poor machinability of halide perovskite crystals severely hampered their practical applications. Here a high-throughput growth method is reported for armored perovskite single-crystal fibers (SCFs). The mold-embedded melt growth (MEG) method provides each SCF with a capillary quartz shell, thus guaranteeing their integrality when cutting and polishing. Hundreds of perovskite SCFs, exemplified by CsPbBr3, CsPbCl3, and CsPbBr2.5I0.5, with customized dimensions (inner diameters of 150-1000 µm and length of several centimeters), are grown in one batch, with all the SCFs bearing homogeneity in shape, orientation, and optical/electronic properties. Versatile assembly protocols are proposed to directly integrate the SCFs into arrays. The assembled array detectors demonstrated low-level dark currents (< 1 nA) with negligible drift, low detection limit (< 44.84 nGy s-1), and high sensitivity (61147 µC Gy-1 cm-2). Moreover, the SCFs as isolated pixels are free of signal crosstalk while showing uniform X-ray photocurrents, which is in favor of high spatial resolution X-ray imaging. As both MEG and the assembly of SCFs involve none sophisticated processes limiting the scalable fabrication, the strategy is considered to meet the preconditions of high-throughput productions.

Sirtuin 1 alleviates neuroinflammation-induced apoptosis after traumatic brain injury.

Sirtuin 1 (SIRT1) plays a very important role in a wide range of biological responses, such as metabolism, inflammation and cell apoptosis. Changes in the levels of SIRT1 have been detected in the brain after traumatic brain injury (TBI). Further, SIRT1 has shown a neuroprotective effect in some models of neuronal death; however, its role and working mechanisms are not well understood in the model of TBI. This study aimed to address this issue. SIRT1-specific inhibitor (sirtinol) and activator (A3) were introduced to explore the role of SIRT1 in cell apoptosis. Results of the study suggest that SIRT1 plays an important role in neuronal apoptosis after TBI by inhibiting NF-κB, IL-6 and TNF-α deacetylation and the apoptotic pathway sequentially, possibly by alleviating neuroinflammation.

Possible mechanism by which renal sympathetic denervation improves left ventricular remodelling after myocardial infarction.

NEW FINDINGS: What is the central question of this study? The enzyme system that is responsible for extracellular matrix (ECM) turnover is the matrix metalloproteinases (MMPs), which can be blocked by the tissue inhibitors of MMPs (TIMPs). Whether renal sympathetic denervation (RSD) is able to ameliorate post-myocardial infarction left ventricular remodelling through attenuation of ECM via regulation of MMP activity and/or the MMP-TIMP complex remains unknown. What is the main finding and its importance? Renal sympathetic denervation has therapeutic effects on post-myocardial infarction left ventricular remodelling, probably by attenuating the ECM through regulation of the MMP9-TIMP1 complex in the transforming growth factor-ß1 (a profibrotic cytokine that accelerates ECM remodelling after ischaemia) signalling pathway. Whether renal sympathetic denervation (RSD) is able to ameliorate post-myocardial infarction (post-MI) left ventricular (LV) remodelling by attenuation of the extracellular matrix via regulation of matrix metalloproteinase (MMP) activity and/or the MMP-tissue inhibitor of matrix metalloproteinase (TIMP) complex remains unknown. Sixty-five Sprague-Dawley rats were randomly divided into the following four groups: normal (N, n = 15), RSD (RSD, n = 15), myocardial infarction (MI, n = 15) and RSD 3 days after MI (MI3d+RSD, n = 20). The bilateral renal nerves were surgically denervated 3 days after MI had been induced by coronary artery ligation. Left ventricular function was assessed using echocardiography and a Millar catheter at 6 weeks post-MI. Plasma noradrenaline, angiotensin II and aldosterone, collagen volume fraction, transforming growth factor-ß1 (TGF-ß1), MMP2, MMP9 and TIMP1 in heart tissue were measured 6 weeks after MI. In rats with MI3d+RSD compared with MI rats, RSD improved systolic and diastolic function, resulting in an improvement in ejection fraction (P < 0.05), fractional shortening (P < 0.05) and LV internal dimension in systole (P < 0.05) and diastole (P < 0.05). Additionally, RSD treatment decreased left ventricular end-diastolic pressure (P < 0.05) and increased LV systolic pressure (P < 0.05) and maximal and minimal rate of LV pressure (both P < 0.05). Meanwhile, RSD reduced collagen content (P < 0.01). TIMP1 was upregulated (P < 0.05), whereas MMP2, MMP9 and TGF-ß1 were downregulated in the LV of RSD-treated animals (P < 0.05). Renal sympathetic denervation has therapeutic effects on post-MI LV remodelling, probably owing to effects on the extracellular matrix by regulation of the MMP9-TIMP1 balance in the TGF-ß1 signalling pathway. Renal sympathetic denervation may be considered as a non-pharmacological approach for the improvement of post-MI cardiac dysfunction.

Intramyocardial delivery of VEGF165 via a novel biodegradable hydrogel induces angiogenesis and improves cardiac function after rat myocardial infarction.

Vascular endothelial growth factor (VEGF), an independent mitogen, has been reported to induce angiogenesis and thus attenuates the damage induced by myocardial infarction (MI). VEGF165 is the most abundant and predominant isoform of VEGF. This study investigates whether this effect could be strengthened by local intramyocardial injection of VEGF165 along with a novel biodegradable Dex-PCL-HEMA/PNIPAAm hydrogel and ascertains its possible mechanism of action. Rat models of myocardial infarction were induced by coronary artery ligation. Phosphate-buffered saline (PBS group), Dex-PCL-HEMA/PNIPAAm hydrogel (Gel group), phosphate-buffered saline containing VEGF165 (VP group), and hydrogel containing VEGF165 (VPG group) were injected into a peri-infarcted area of cardiac tissue immediately after myocardial infarction, respectively. The sham group was thoracic but without myocardial infarction. The injection of VEGF165 along with a hydrogel induced angiogenesis, reduced collagen content and MI area, inhibited cell apoptosis, increased the level of VEGF165 protein and the expression of flk-1 and flt-1, and improved cardiac function compared with the injection of either alone after MI in rats. The results suggest that injection of VEGF165 along with a hydrogel acquires more cardioprotective effects than either alone in rat with MI by sustained release of VEGF165, then may enhance the feedback between VEGF and its receptors flk-1 and flt-1.

Renal Sympathetic Denervation in Rats Ameliorates Cardiac Dysfunction and Fibrosis Post-Myocardial Infarction Involving MicroRNAs.

BACKGROUND The role of renal sympathetic denervation (RSD) in ameliorating post-myocardial infarction (MI) left ventricular (LV) fibrosis via microRNA-dependent regulation of connective tissue growth factor (CTGF) remains unknown. MATERIAL AND METHODS MI and RSD were induced in Sprague-Dawley rats by ligating the left coronary artery and denervating the bilateral renal nerves, respectively. Norepinephrine, renin, angiotensin II and aldosterone in plasma, collagen, microRNA21, microRNA 101a, microRNA 133a and CTGF in heart tissue, as well as cardiac function were evaluated six weeks post-MI. RESULTS In the RSD group, parameters of cardiac function were significantly improved as evidenced by increased LV ejection fraction (p<0.01), LV end-systolic diameter (p<0.01), end-diastolic diameter (p<0.05), LV systolic pressure (p<0.05), maximal rate of pressure rise and decline (dP/dtmax and dP/dtmin, p<0.05), and decreased LV end-diastolic pressure (p<0.05) when compared with MI rats. Further, reduced collagen deposition in peri-infarct myocardium was observed in RSD-treated rats along with higher microRNA101a and microRNA133a (p<0.05) and lower microRNA21 expression (p<0.01) than in MI rats. CTGF mRNA and protein levels were decreased in LV following RSD (p<0.01), accompanied by decreased expression of norepinephrine, renin, angiotensin II and aldosterone in plasma (p<0.05) compared with untreated MI rats. CONCLUSIONS The potential therapeutic effects of RSD on post-MI LV fibrosis may be partly mediated by inhibition of CTGF expression via upregulation of microRNA 101a and microRNA 133a and downregulation of microRNA21.

In situ imaging of on-surface, solvent-free molecular single-crystal growth.

The formation of crystalline materials has been studied for more than a century. Recent discoveries about the self-assembly of many inorganic materials, involving aggregation of nanoparticle (NP) precursors or pre-nucleation clusters, challenge the simple assumptions of classical crystallization theory. The situation for organic materials is even more of a terra incognita due to their high complexity. Using in situ high-temperature atomic force microscopy during the solvent-free crystallization of an organic compound [Ni(quinolone-8-thiolate)2], we observe long-range migration of NPs on a silica substrate and their incorporation into larger crystals, suggesting a non-classical pathway in the growth of the molecular crystal.

In Situ Microscopic Observation of the Crystallization Process of Molecular Microparticles by Fluorescence Switching.

To clearly understand the solid-state amorphous-to-crystalline transformation is a long-standing challenge because such crystallization occuring in confined environments is difficult to observe directly. We developed an in situ and real-time imaging procedure to record the interface evolution in a solid-state crystallization of molecular amorphous particles. The method, by employing a tetra-substituted ethene with novel morphology-dependent fluorescence, which can distinguish the interfaces between the crystalline and amorphous phase by fluorescence color, is a simple and practical method to probe the inner process of a molecular microparticle. The crystallization of amorphous microparticles in different cases was clearly recorded, where the perfect microparticles and those with defects demonstrate diverse destinies. The details disclosed in this observation will deepen the understanding for a series of solid-state crystallization that we know little about before.

Novel pyrazoline-based selective fluorescent sensor for Hg2+.

This paper presents the preparation of a pyrazoline compound and the properties of its UV-Vis absorption and fluorescence emission. Moreover, this compound can be used to determine Hg(2+) ion with selectivity and sensitivity in the EtOH:H2O =9:1 (v/v) solution. This sensor forms a 1:1 complex with Hg(2+) and shows a fluorescent enhancement with good tolerance of other metal ions. This sensor is very sensitive with fluorometric detection limit of 3.85 × 10(-10) M. In addition, the fluorescent probe has practical application in cells imaging.

Exogenous high-mobility group box 1 protein prevents postinfarction adverse myocardial remodeling through TGF-ß/Smad signaling pathway.

High-mobility group box 1 (HMGB1) has been reported to attenuate ventricular remodeling, but its mechanism remains mostly unresolved. Transforming growth factor-beta (TGF-ß) is a crucial mediator in the pathogenesis of post-infarction remodeling. Our study focused on the effects of HMGB1 on ventricular remodeling, and explored whether or not these effects were depended upon the TGF-ß signaling pathway. Rats underwent coronary artery ligation. An intramyocardium injection of phosphate buffered saline (PBS) with or without HMGB1 was administered 3 weeks after myocardial infarction (MI). At 4 weeks after the treatment, HMGB1 significantly increased the left ventricular ejection fraction (LVEF) (P < 0.05), decreased the left ventricular end diastolic dimension (LVEDD; P < 0.05), left ventricular end systolic dimension (LVESD) (P < 0.05) and the infarct size (P < 0.05) compared with control group. The expressions of collagen I, collagen III, and tissue inhibitor of metalloproteinase 2 (TIMP2) were also decreased, while the matrix metalloproteinases 2 (MMP2) and MMP9 expressions were upregulated by HMGB1 injection (P < 0.05) compared with control group. No effect on TIMP3 was observed. Furthermore, TGF-ß1 and phosphor-Smad2 (p-Smad2) were significantly suppressed and Smad7 was increased in HMGB1-treated group (P < 0.05) compared with control group, no effects on p-Smad3 and p-p38 were observed. HMGB1 also upregulated Smad 7 expression and decreased the level of collagen I on cardiac fibroblasts (P < 0.05). Silencing of Smad7 gene by small interfering RNA abolished the fibrogenic effects of HMGB1 on cardiac fibroblasts (P < 0.05). These finding suggested that HMGB1 injection modulated ventricular remodeling may function through the possible inhibition of TGF-ß/Smad signaling pathway.

Intramyocardial delivery of HMGB1 by a novel thermosensitive hydrogel attenuates cardiac remodeling and improves cardiac function after myocardial infarction.

BACKGROUND: High-mobility group box 1 (HMGB1), a nuclear protein, has been recently reported to attenuate cardiac remodeling after myocardial infarction (MI). This study was designed to investigate whether this effect could be strengthened by local intramyocardial injection of HMGB1 along with a novel Dex-PCL-HEMA/PNIPAAm hydrogel and ascertain its possible mechanism of action. METHODS: Rat models were induced by coronary artery ligation. Phosphate-buffered solution, Dex-PCL-HEMA/PNIPAAm hydrogel, HMGB1 in phosphate-buffered solution, or HMGB1 in hydrogel was injected into a peri-infarcted area of cardiac tissue immediately after MI. RESULTS: The injection of HMGB1 along with hydrogel improved cardiac function and reduced collagen content. Additionally, the number of c-Kit/Ki67, α-sarcomeric/MEF2C, and α-sarcomeric/Ki67 cells were increased significantly compared with the results of using either agent alone. CONCLUSIONS: HMGB1 injection with Dex-PCL-HEMA/PNIPAAm hydrogel attenuates cardiac remodeling and improves cardiac function after MI by inducing myocardial regeneration.

A novel pyrazoline-based selective fluorescent probe for detecting reduced glutathione and its application in living cells and serum.

A new fluorescent probe, N-(4-(1,5-diphenyl-4,5-dihydro-1H-pyrazol-3-yl)phenyl)-2,4-dinitrobenzenesulfonamide (probe 3), was designed and synthesized as a highly sensitive and selective fluorescent probe for recognizing and detecting glutathione among biological thiols in aqueous media. Probe 3 is a nonfluorescent compound. On being mixed with biothiols under neutral aqueous conditions, the 2,4-dinitrobenzenesulfoyl moiety can be cleaved off by glutathione, and the blue emission of the pyrazoline at 464 nm is switched on, with a fluorescence enhancement of 488-fold for glutathione. Furthermore, probe 3 was highly selective for glutathione without interference from some biologically relevant analytes. The detection limit of glutathione was 4.11 × 10(-7) M. The emission of the probe is pH independent in the physiological pH range. Moreover, the probe can be used for fluorescent imaging of cellular glutathione and can be used for detecting glutathione in calf serum.

Polymer-Assisted Compressed Flux Growth: A Universal and High-Yield Method for Dimension-Controlled Single Crystals.

Single crystals possess the most perfect and stable morphology and represent the intrinsic and upper limits of performance when integrated into various application scenarios. However, for a large portion of the newly emerging low-dimensional and molecular materials, the mass production of crystals with a desirable shape is still challenging. Here, a universal and high-yield method to grow functional single crystals with controlled dimensions is provided that can be directly integrated into a device. By utilizing a polymeric flux in combination with a compressed growth space, numerous materials can be grown into size-controllable single crystalline flakes, with millions produced in one batch. This scalable growth method shows promise for the large-scale integration of micro-single-crystals as functional components, as exemplified by the construction of a 5 in. field-effect transistor array.

Germacrone mitigates cardiac remodeling by regulating PI3K/AKT-mediated oxidative stress, inflammation, and apoptosis.

Cardiac remodeling is a common consequence of cardiovascular diseases and is closely associated with oxidative stress, inflammation, and apoptosis. Germacrone, a bioactive compound present in Rhizoma curcuma, has been shown to possess anti-oxidative, anti-inflammatory, and anti-apoptotic properties. The aim of this study was to investigate the protective effect of germacrone against cardiac remodeling. Here, C57BL/6 mice were subcutaneous injection with isoproterenol (ISO) once daily for two weeks and were concurrent intragastric injection of germacrone. In vitro, neonatal rat cardiomyocytes (NRCMs) were used to verify the protective effect of germacrone on ISO-induced cardiac injury. Our findings indicated that ISO induce oxidative stress, inflammation, and apoptosis in vivo and in vitro, while germacrone treatment significantly attenuates these effects, thereby attenuating myocardium remodeling and cardiac dysfunction. Mechanistically, germacrone reduced cardiac remodeling-induced activation of phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway, and the cardioprotective effects of germacrone were abrogated by a PI3K agonist. In conclusion, our results suggest that germacrone attenuates oxidative stress, inflammation, and apoptosis in cardiac remodeling by inhibiting the PI3K/AKT pathway, and may therefore represent a promising therapeutic approach for the treatment of cardiac remodeling.

Burden of type 1 and type 2 diabetes and high fasting plasma glucose in Europe, 1990-2019: a comprehensive analysis from the global burden of disease study 2019.

Introduction: With population aging rampant globally, Europe faces unique challenges and achievements in chronic disease prevention. Despite this, comprehensive studies examining the diabetes burden remain absent. We investigated the burden of type 1 and type 2 diabetes, alongside high fasting plasma glucose (HFPG), in Europe from 1990-2019, to provide evidence for global diabetes strategies. Methods: Disease burden estimates due to type 1 and type 2 diabetes and HFPG were extracted from the GBD 2019 across Eastern, Central, and Western Europe. We analyzed trends from 1990 to 2019 by Joinpoint regression, examined correlations between diabetes burden and Socio-demographic indices (SDI), healthcare access quality (HAQ), and prevalence using linear regression models. The Population Attributable Fraction (PAF) was used to described diabetes risks. Results: In Europe, diabetes accounted for 596 age-standardized disability-adjusted life years (DALYs) per 100,000 people in 2019, lower than globally. The disease burden from type 1 and type 2 diabetes was markedly higher in males and escalated with increasing age. Most DALYs were due to type 2 diabetes, showing regional inconsistency, highest in Central Europe. From 1990-2019, age-standardized DALYs attributable to type 2 diabetes rose faster in Eastern and Central Europe, slower in Western Europe. HFPG led to 2794 crude DALYs per 100,000 people in 2019. Type 1 and type 2 diabetes burdens correlated positively with diabetes prevalence and negatively with SDI and HAQ. High BMI (PAF 60.1%) and dietary risks (PAF 34.6%) were significant risk factors. Conclusion: Europe's diabetes burden was lower than the global average, but substantial from type 2 diabetes, reflecting regional heterogeneity. Altered DALYs composition suggested increased YLDs. Addressing the heavy burden of high fasting plasma glucose and the increasing burden of both types diabetes necessitate region-specific interventions to reduce type 2 diabetes risk, improve healthcare systems, and offer cost-effective care.

Morphology dependent light-induced photoluminescence enhancement of CsPbBr3 microcrystals.

Herein, we report a facile method for growing CsPbBr3 cube and prism microcrystals by microspacing in-air sublimation. Morphology-dependent photoluminescence behavior investigation reveals that the CsPbBr3 cubes show higher photoluminescence quantum yield and longer PL lifetime than the prisms. In contrast, CsPbBr3 prisms exhibit more considerable light-induced photoluminescence enhancement.

Changing trends of disease burden of stroke from 1990 to 2019 and its predictions among the Chinese population.

Objective: This study aimed to understand the temporal trends in the disease burden of stroke and its attributable risk factors in China, along with the future trends in the next 25 years, that is important for effective prevention strategies and improvement, and to provide new insights into the age- and sex-specific incidence, prevalence, mortality, disability-adjusted life-years (DALYs) and their trends from 1990 to 2019, and the prediction in the next 25 years. Methods: The Global Burden of Disease Study (2019) was used to extract the data on age- and sex-specific incidence, mortality, and disability-adjusted life-years (DALYs) of stroke in China, 1990-2019. We estimated the estimated annual percentage change (EAPC) to access the temporal trends of the disease burden of stroke. The R package called Nordpred was used to perform an age-period-cohort analysis to predict the prevalence of stroke. Results: The number of incidence cases, deaths, and DALYs of stroke increased from 1990 to 2019. Overall downward trends were observed in the age-standardized incidence rate (ASIR) from 1990 to 2019. Significant temporal trends in mortality and DALYs of stroke were observed. High systolic blood pressure, smoking, and high-sodium diet were the main driving forces for stroke. The DALYs lost attributable to smoking were different for male and female patients. In the next 25 years, the number of new cases and deaths from stroke should continue to increase. The ASIR and age-standardized mortality rate (ASMR) should show a downward trend among male and female patients. Conclusion: Despite the overall rates of stroke declined over the period from 1990 to 2019, the absolute number of people affected by stroke has substantially increased. There has been a substantial increase in the burden of stroke due to risk factors and will continue to increase in the next 25 years.

A processable, scalable, and stable full-color ultralong afterglow system based on heteroatom-free hydrocarbon doped polymers.

Although room-temperature phosphorescence (RTP) organic materials are a widely-studied topic especially popular in recent decades, long-lived RTP able to fulfil broad time-resolved application requirements reliably, are still rare. Polymeric materials doped with phosphorescent chromophores generally feature high productivity and diverse applications, compared with their crystalline counterparts. This study proves that pure polycyclic aromatic hydrocarbons (PAHs) may even outperform chromophores containing hetero- or heavy-atoms. Full-color (blue, green, orange and red) polymer-PAHs with lifetimes >5000 ms under ambient conditions are constructed, which provide impressive values compared to the widely reported polymer-based RTP materials in the respective color regions. The polymer-PAHs could be fabricated on a large-scale using various methods (solution, melt and in situ polymerization), be processed into diverse forms (writing ink, fibers, films, and complex 3D architectures), and be used in a range of applications (anti-counterfeiting, information storage, and oxygen sensors). Plus their environmental (aqueous) stability makes the polymer-PAHs a promising option to expand the portfolio of organic RTPs.

Homogeneously Oriented Organic Single-Crystalline Patterns Grown by Microspacing In-Air Sublimation.

Fabrication of single-crystalline organic semiconductor patterns is of key importance to enable practical applications. However due to the poor controllability on nucleation locations and the intrinsic anisotropic nature of single-crystals, growth of single-crystal patterns with homogeneous orientation is a big challenge especially by the vapor method. Herein a vapor growth protocol to achieve patterned organic semiconductor single-crystals with high crystallinity and uniform crystallographic orientation is presented. The protocol relies on the recently invented microspacing in-air sublimation assisted with surface wettability treatment to precisely pin the organic molecules at desired locations, and inter-connecting pattern motifs to induce homogeneous crystallographic orientation. Single-crystalline patterns with different shapes and sizes, and uniform orientation are demonstrated exemplarily by using 2,7-dioctyl[1]benzothieno[3,2-b][1]benzothiophene (C8-BTBT). Field-effect transistor arrays fabricate on the patterned C8-BTBT single-crystal patterns show uniform electrical performance: a 100% yield with an average mobility of 6.28 cm2  V-1  s-1 and in a 5 × 8 array. The developed protocols overcome the uncontrollability of the isolated crystal patterns in vapor growth on non-epitaxial substrates, making it possible to align the anisotropic electronic nature of single-crystal patterns in large-scale devices integration.

Changing trends of the disease burden of non-rheumatic valvular heart disease in China from 1990 to 2019 and its predictions: Findings from global burden of disease study.

Objective: China has an increasing burden of non-rheumatic valvular heart disease (NRVHD) as the aging of the population is deepening. The aim was to assess the age and sex-specific prevalence and DALYs of NRVHD in China from 1990 to 2019 and to predict the burden in the next 25 years. Methods: The Global Burden of Disease Study (2019) was used to extract the data of age- and sex-specific incidence, mortality, and disability-adjusted life years (DALYs) of NRVHD in China, 1990-2019. We estimated the annual percentage change (EAPC) to access the temporal trends of the disease burden of NRVHD. The R package called Nordpred was used to perform an age-period-cohort analysis to predict the prevalence of NRVHD in the next 25 years. Results: The number of incident cases of NRVHD increased from 93.16 thousand in 1990 to 325.05 thousand in 2019. Overall upward trends were observed in the age-standardized incidence rate (ASIR) from 1990 to 2019. Significant temporal trends in mortality and DALYs of NRVHD were observed. High systolic blood pressure, high sodium diet, and lead exposure were the main driving forces for NRVHD. In the next 25 years, the number of new cases and deaths of NRVHD should continue to increase to 390.64 thousand and 10.0 thousand, respectively. The ASIR should show an upward trend, while the ASMR should show a downward trend among men and women. Conclusion: In China, the overall rates of NRVHD have increased over the past 30 years, and there has been a substantial increase in the burden of NRVHD due to population growth and aging and will continue to increase in the next 25 years. Our results can help shape a multifactorial approach and public policy to reduce the NRVHD burden throughout China.

The factors influencing the efficiency of drug-coated balloons.

The drug-coated balloon (DCB) is an emerging percutaneous coronary intervention (PCI) device that delivers drugs to diseased vessels to decrease the rate of vascular stenosis. Recent clinical studies have demonstrated that DCBs tend to have both good safety and efficacy profiles, leading to extended application indications in the clinic, including in-stent restenosis (ISR) for metal stents such as drug-eluting stents (DESs), small vascular disease, bifurcation disease, large vascular disease, acute coronary syndrome (ACS), and high bleeding risk. However, some previous clinical data have suggested that DCBs performed less effectively than DESs. No studies or reviews have systematically discussed the improvement strategies for better DCB performance until now. Drug loss during the process of delivery to the target lesion and inefficient delivery of the coating drug to the diseased vascular wall are two key mechanisms that weaken the efficiency of DCBs. This review is the first to summarize the key influencing factors of DCB efficiency in terms of balloon structure and principles, and then it analyzes how these factors cause outcomes in practice based on current clinical trial studies of DCBs in the treatment of different types of lesions. We also provide some recommendations for improving DCBs to contribute to better DCB performance by improving the design of DCBs and combining other factors in clinical practice.