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The fine particulate matter (PM2.5) in air pollution is a critical risk factor influencing human health. Our study included 8144 participants and showed that the risk of major adverse cardiovascular events increases by 35% (HR, 1.35; 95% CI, 1.14-1.60) for participants with the highest quartile to PM2.5 exposure as compared to those with lowest quartile. Bioaerosols, as an important environmental exposure in PM2.5, can induce systemic chronic inflammation leading to vascular aging. Thus, the effects of bioaerosols are investigated from household garbage stations in PM2.5 on vascular aging, and the underlying mechanisms are explored. In vivo, chronic exposure to bioaerosols upregulated senescence marker expression levels while causing vascular dysfunction and remodeling. In vitro, bioaerosol exposure induced decreased proliferation, G0/G1 arrest, and impaired migration of human umbilical vein endothelial cells (HUVECs). Furthermore, a single bacterium (AS22a) from the bioaerosol community was isolated and demonstrated that it upregulated inflammatory factors and accelerated cell senescence and vascular aging by activating the NF-κB/NLRP3 signaling pathway, which may serve as a primary mechanism underlying vascular aging induced by bioaerosols in PM2.5. These findings suggest that high levels of bioaerosols in household garbage stations may adversely affect cardiovascular health., (© 2024 The Author(s). Advanced Science published by Wiley‐VCH GmbH.)

The high incidence of restenosis after angioplasty has been the leading reason for the recurrence of coronary heart disease, substantially increasing the mortality risk for patients. However, current anti-stenosis drug-eluting stents face challenges due to their limited functions and long-term safety concerns, significantly compromising their therapeutic effect. Herein, a stent-free anti-stenosis drug coating (denoted as Cur-NO-Gel) based on a peptide hydrogel is proposed. This hydrogel is formed by assembling a nitric oxide (NO) donor-peptide conjugate as a hydrogelator and encapsulating curcumin (Cur) during the assembly process. Cur-NO-Gel has the capability to release NO upon β-galactosidase stimulation and gradually release Cur through hydrogel hydrolysis. The in vitro experiments confirmed that Cur-NO-Gel protects vascular endothelial cells against oxidative stress injury, inhibits cellular activation of vascular smooth muscle cells, and suppresses adventitial fibroblasts. Moreover, periadventitial administration of Cur-NO-Gel in the angioplasty model demonstrate its ability to inhibit vascular stenosis by promoting reendothelialization, suppressing neointima hyperplasia, and preventing constrictive remodeling. Therefore, the study provides proof of concept for designing a new generation of clinical drugs in angioplasty., (© 2024 The Authors. Advanced Science published by Wiley‐VCH GmbH.)

Coevolution of tumor cells and surrounding stroma results in protective protumoral environment, in which abundant vessel, stiff structure and immunosuppression promote each other, cooperatively incurring deterioration and treatment compromise. Reversing suchenvironment may transform tumors from treatment-resistant to treatment-vulnerable. However, effective reversion requires synergistic comprehensive regression of such environment under precise control. Here, the first attempt to collaboratively retrograde coevolutionary tumor environment to pre-oncogenesis status, defined as tumor environment regression therapy, is made for vigorous immune response eruption by a switchable prune-to-essence nanoplatform (Pres) with simplified composition and fabrication process. Through magnetic targeting and multimodal imaging of Pres, tumor environment regression therapy is guided, optimized and accomplished in a trinity way: Antiangiogenesis is executed to rarefy vessels to impede tumor progression. By seizing the time, cancer associated fibroblasts are eliminated to diminish collagen and loosen the stiff structure for deep penetration of Pres, which alternately functioned in deeper tumors, forming a positive feedback loop. Through this loop, immune cell infiltration, immunosuppression mitigation and immunogenic cells death induction are all fulfilled and further escalated in the regressed environment. These transformations consequently unleashed systemic immune responses and generated immune memory against carcinoma. This study provides new insights intotreatment of solid tumors., (© 2023 The Authors. Advanced Science published by Wiley-VCH GmbH.)

Excessive or persistent inflammation incites cardiomyocytes necrosis by generating reactive oxygen species in myocardial infarction (MI). Hydrogen sulfide (H 2 S), a gaseous signal molecule, can quickly permeate cells and tissues, growing concerned for its cardioprotective effects. However, short resident time and strong side effects greatly restrict its application. Herein, a complex scaffold (AAB) is first developed to slowly release H 2 S for myocardial protection by integrating alginate modified with 2-aminopyridine-5-thiocarboxamide (H 2 S donor) into albumin electrospun fibers. Next, a band-aid like patch is constructed based on AAB (center) and nanocomposite scaffold which comprises albumin scaffold and black phosphorus nanosheets (BPNSs). With near-infrared laser (808 nm), thermal energy generated by BPNSs can locally change the molecular structure of fibrous scaffold, thereby attaching patch to the myocardium. In this study, it is also demonstrated that AAB can enhance regenerative M2 macrophage and attenuate inflammatory polarization of macrophages via reduction in intracellular ROS. Eventually, this engineered cardiac patch can relieve inflammation and promote angiogenesis after MI, and thereby recover heart function, providing a promising therapeutic strategy for MI treatment., (© 2022 The Authors. Advanced Science published by Wiley-VCH GmbH.)

Cancer patients often face severe organ toxicity caused by chemotherapy. Among these, chemotherapy-induced hepatotoxicity and cardiotoxicity are the main causes of death of cancer patients. Chemotherapy-induced cardiotoxicity even creates a new discipline termed "cardio-oncology". Therefore, relieving toxicities induced by chemotherapy has become a key issue for improving the survival and quality of life in cancer patients. In this work, mesenchymal stem cell exosomes with the "G-C" abundant tetrahedral DNA nanostructure (TDN) are modified to form a decoy exosome (Exo-TDN). Exo-TDN reduces DOX-induced hepatotoxicity as the "G-C" base pairs scavenge DOX. Furthermore, Exo-TDN with cardiomyopathic peptide (Exo-TDN-PCM) is engineered for specific targeting to cardiomyocytes. Injection of Exo-TDN-PCM significantly reduces DOX-induced cardiotoxicity. Interestingly, Exo-TDN-PCM can also promote macrophage polarization into the M2 type for tissue repair. In addition, those decoy exosomes do not affect the anticancer effects of DOX. This decoy exosome strategy serves as a promising therapy to reduce chemo-induced toxicity., (© 2022 The Authors. Advanced Science published by Wiley-VCH GmbH.)

Environmentally benign and potentially cost-effective Sb 2 Se 3 solar cells have drawn much attention by continuously achieving new efficiency records. This article reports a compatible strategy to enhance the efficiency of planar n-i-p Sb 2 Se 3 solar cells through Sb 2 Se 3 surface modification and an architecture with oriented 1D van der Waals material, trigonal selenium (t-Se). A seed layer assisted successive close spaced sublimation (CSS) is developed to fabricate highly crystalline Sb 2 Se 3 absorbers. It is found that the Sb 2 Se 3 absorber exhibits a Se-deficient surface and negative surface band bending. Reactive Se is innovatively introduced to compensate the surface Se deficiency and form an (101) oriented 1D t-Se interlayer. The p-type t-Se layer promotes a favored band alignment and band bending at the Sb 2 Se 3 /t-Se interface, and functionally works as a surface passivation and hole transport material, which significantly suppresses interface recombination and enhances carrier extraction efficiency. An efficiency of 7.45% is obtained in a planar Sb 2 Se 3 solar cell in superstrate n-i-p configuration, which is the highest efficiency for planar Sb 2 Se 3 solar cells prepared by CSS. The all-inorganic Sb 2 Se 3 solar cell with t-Se shows superb stability, retaining ≈98% of the initial efficiency after 40 days storage in open air without encapsulation., Competing Interests: The authors declare no conflict of interest., (© 2020 The Authors. Published by WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim.)

[This corrects the article DOI: 10.1002/advs.201801260.]., (© 2020 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim.)

As a transcription coactivator, Yes-associated protein 1 (YAP1)'s role in tumorigenesis is well established. However, the mechanism of YAP1-regulating long noncoding RNAs (lncRNA) in tumors is still largely unknown. Here, a YAP1 target gene, long intergenic noncoding RNA 00152 (LINC00152), which is highly expressed in colorectal cancer (CRC), is identified. The oncogenic functions of LINC00152 in CRC are demonstrated by a panel of in vitro and in vivo experiments. Further studies reveal the potential downstream mechanisms of LINC00152, which can act as a competing endogenous RNA sponging with miR-632 and miR-185-3p to regulate Fascin actin-bundling protein 1 (FSCN1) expression and thus promote the malignant proliferation and metastasis in CRC cells. Targeting the YAP1/LINC00152/FSCN1 axis inhibits the progression of CRC. This finding provides a new regulatory model of the "YAP1-lncRNA" in CRC, which gives rise to a new perspective, "YAP1/LINC00152/miR-632-miR-185-3p/FSCN1," to explore the cancer-promoting mechanism of YAP1 involved in CRC., Competing Interests: The authors declare no conflict of interest., (© 2019 The Authors. Published by WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim.)

Although numerous therapies are widely applied clinically and stem cells and/or biomaterial based in situ implantations have achieved some effects, few of these have observed robust myocardial regeneration. The beneficial effects on cardiac function and structure are largely acting through paracrine signaling, which preserve the border-zone around the infarction, reduce apoptosis, blunt adverse remodeling, and promote angiogenesis. Ionic extracts from biomaterials have been proven to stimulate paracrine effects and promote cell-cell communications. Here, the paracrine stimulatory function of bioactive ions derived from biomaterials is integrated into the clinical concept of administration and proposed "ion therapy" as a novel strategy for myocardial infarction. In vitro, silicon- enriched ion extracts significantly increase cardiomyocyte viability and promote cell-cell communications, thus stimulating vascular formation via a paracrine effect under glucose/oxygen deprived conditions. In vivo, by intravenous injection, the bioactive silicon ions act as "diplomats" and promote crosstalk in myocardial cells, stimulate angiogenesis, and improve cardiac function post-myocardial infarction.