Peptide amphiphiles alleviate myocardial endoplasmic reticulum stress to enhance cardiomyocyte-macrophage communication and promote macrophage M2 polarization.

Myocardial ischemia-reperfusion (I/R) injury represents a significant clinical challenge with limited therapeutic options. Single-cell RNA sequencing and bioinformatics analyses have revealed complex cellular interactions within cardiac tissue, highlighting the crucial role of cardiomyocytes in intercellular communication. During I/R injury, cardiomyocytes experience severe endoplasmic reticulum (ER) stress, leading to detrimental intercellular communication that affects surrounding cells, particularly promoting the transformation of macrophages toward a pro-inflammatory phenotype.

Legumain-Guided Ferulate-Peptide Self-Assembly Enhances Macrophage-Endotheliocyte Partnership to Promote Therapeutic Angiogenesis After Myocardial Infarction.

Promoting angiogenesis and modulating the inflammatory microenvironment are promising strategies for treating acute myocardial infarction (MI). Macrophages are crucial in regulating inflammation and influencing angiogenesis through interactions with endothelial cells. However, current therapies lack a comprehensive assessment of pathological and physiological subtleties, resulting in limited myocardial recovery.

Optimized Two-Photon Imaging by Stimuli-Responsive Peptide Self-Assembly Facilitates Self-Assisted Counteraction of Cisplatin-Resistance in Cancer Cells.

Accurate diagnosis and effective treatment of tumors remain significant clinical challenges. While fluorescence imaging is essential for tumor detection, it has limitations in terms of specificity, penetration depth, and emission wavelength. Here, we report a novel glutathione (GSH)-responsive peptide self-assembly excimer probe () that optimizes two-photon tumor imaging and self-assisted counteraction of the cisplatin resistance in cancer cells.

An in-situ peptide-antibody self-assembly to block CD47 and CD24 signaling enhances macrophage-mediated phagocytosis and anti-tumor immune responses.

Targeted immunomodulation for reactivating innate cells, especially macrophages, holds great promise to complement current adaptive immunotherapy. Nevertheless, there is still a lack of high-performance therapeutics for blocking macrophage phagocytosis checkpoint inhibitors in solid tumors. Herein, a peptide-antibody combo-supramolecular in situ assembled CD47 and CD24 bi-target inhibitor (PAC-SABI) is described, which undergoes biomimetic surface propagation on cancer cell membranes through ligand-receptor binding and enzyme-triggered reactions.

Adaptive enzyme-responsive self-assembling multivalent apelin ligands for targeted myocardial infarction therapy.

Microvascular dysfunction following myocardial infarction exacerbates coronary flow obstruction and impairs the preservation of ventricular function. The apelinergic system, known for its pleiotropic effects on improving vascular function and repairing ischemic myocardium, has emerged as a promising therapeutic target for myocardial infarction. Despite its potential, the natural apelin peptide has an extremely short circulating half-life.

Dual-crosslinking immunostimulatory hydrogel synchronously suppresses pancreatic fistula and pancreatic cancer relapse post-resection.

In pancreatic cancer (PC), surgical resection remains the sole curative option, albeit patients undergoing resection are susceptible to postoperative pancreatic fistula (PF) formation and tumor recurrence. An unmet need exists for a unified strategy capable of concomitantly averting PF and tumor relapse to mitigate morbidity in PC patients after surgery. Herein, an original dual crosslinked biological sealant hydrogel (methacrylate-hyaluronic acid-dopamine (MA-HA-DA) and sulfhydryl-hyaluronic acid-dopamine (SH-HA-DA)) was engineered as a drug depot and loaded with polydopamine-cloaked cytokine interleukin-15 and platelets conjugated with anti-TIGIT.

Baicalin-peptide supramolecular self-assembled nanofibers effectively inhibit ferroptosis and attenuate doxorubicin-induced cardiotoxicity.

Doxorubicin, an anthracycline chemotherapeutic agent, elicits a deleterious cardiotoxicity known as doxorubicin-induced cardiomyopathy (DIC) that circumscribes its chemotherapy utility for malignancies. Recent empirical evidence implicates ferroptosis, an iron-dependent form of regulated cell death, as playing a pivotal role in the pathogenesis of DIC. We postulated that anti-ferroptosis agents may constitute a novel therapeutic strategy for mitigating DIC.

Supramolecular Peptide Amphiphile Nanospheres Reprogram Tumor-associated Macrophage to Reshape the Immune Microenvironment for Enhanced Breast Cancer Immunotherapy.

Tumor immunotherapy has become a research hotspot in cancer treatment, with macrophages playing a crucial role in tumor development. However, the tumor microenvironment restricts macrophage functionality, limiting their therapeutic potential. Therefore, modulating macrophage function and polarization is essential for enhancing tumor immunotherapy outcomes.

Guiding ablation strategies for ventricular tachycardia in patients with structural heart disease by analyzing links and conversion patterns of traceable abnormal late potential zone.

Background: Substrate-based ablation can treat uninducible or hemodynamically instability scar-related ventricular tachycardia (VT). However, whether a correlation exists between the critical VT isthmus and late activation zone (LAZ) during sinus rhythm (SR) is unknown.

Objective: To demonstrate the structural and functional properties of abnormal substrates and analyze the link between the VT circuit and abnormal activity during SR.

Supramolecular Assemblies of Glycopeptides Enhance Gap Junction Maturation of Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes via Inducing Spheroids Formation to Optimize Cardiac Repair.

Stem cell-based therapies have demonstrated significant potential for use in heart regeneration. An effective paradigm for heart repair in rodent and large animal models is the transplantation of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). Despite this, the functional and phenotypical immaturity of 2D-cultured hiPSC-CMs, particularly their low electrical integration, poses a caveat for clinical translation.

Islet-1 Mesenchymal Stem Cells-Derived Exosome-Incorporated Angiogenin-1 Hydrogel for Enhanced Acute Myocardial Infarction Therapy.

Although stem cell-derived exosomes have been recognized as new candidates for cell-free treatment in myocardial infarction (MI), the challenge to improve the exosome retention in ischemic tissue remains. Our previous research indicated that islet-1(ISL1) overexpression enhances the paracrine function of mesenchymal stem cells (MSCs) and promotes angiogenesis in a model of MI. In this study, genetically engineered ISL1-MSC-derived exosomes (ISL1-MSCs-Exo) were collected, and the contents were analyzed by exosomal RNA sequencing.

An injectable co-assembled hydrogel blocks reactive oxygen species and inflammation cycle resisting myocardial ischemia-reperfusion injury.

The overproduction of reactive oxygen species (ROS) and burst of inflammation following cardiac ischemia-reperfusion (I/R) are the leading causes of cardiomyocyte injury. Monotherapeutic strategies designed to enhance anti-inflammatory or anti-ROS activity explicitly for treating I/R injury have demonstrated limited success because of the complex mechanisms of ROS production and induction of inflammation. Intense oxidative stress leads to sustained injury, necrosis, and apoptosis of cardiomyocytes.

Roles of Ferroptosis in Cardiovascular Diseases.

Ferroptosis is an iron-dependent regulated cell death characterized by lipid peroxidation and iron overload, which is different from other types of programmed cell death, including apoptosis, necroptosis, autophagy, and pyroptosis. Over the past years, emerging studies have shown a close relation between ferroptosis and various cardiovascular diseases such as atherosclerosis, acute myocardial infarction, ischemia/reperfusion injury, cardiomyopathy, and heart failure. Herein, we will review the contributions of ferroptosis to multiple cardiovascular diseases and the related targets.

Robust drug bioavailability and safety for rheumatoid arthritis therapy using D-amino acids-based supramolecular hydrogels.

Long-term use of disease-modifying anti-rheumatic drugs (DMARDs) such as methotrexate (MTX) shows clinical benefits for rheumatoid arthritis (RA) treatment. However, there are growing concerns over the adverse effects of systemic drug administration. Therefore, a strategy that can enhance drug bioavailability while minimizing side effects is urgently needed, but remains a challenge in RA therapy.

Organelle-inspired supramolecular nanomedicine to precisely abolish liver tumor growth and metastasis.

Organelles are responsible for the efficient storage and transport of substances in living systems. A myriad of extracellular vesicles (EVs) acts as a bridge to exchange signaling molecules in cell-cell communication, and the highly dynamic tubulins and actins contribute to efficient intracellular substance transport. The inexhaustible cues of natural cargo delivery by organelles inspire researchers to explore the construction of biomimetic architectures for "smart" delivery carriers.

Injectable AuNP-HA matrix with localized stiffness enhances the formation of gap junction in engrafted human induced pluripotent stem cell-derived cardiomyocytes and promotes cardiac repair.

Cell therapy offers a promising paradigm for heart tissue regeneration. Human induced pluripotent stem cells (hiPS) and their cardiac derivatives are emerging as a novel treatment for post-myocardial infarction repair. However, the immature phenotype and function of hiPS-derived cardiomyocytes (hiPS-CMs), particularly poor electrical coupling, limit their potential as a therapy.

Correction: Furin-instructed molecular self-assembly actuates endoplasmic reticulum stress-mediated apoptosis for cancer therapy.

Correction for 'Furin-instructed molecular self-assembly actuates endoplasmic reticulum stress-mediated apoptosis for cancer therapy' by Chenxing Fu et al., Nanoscale, 2020, 12, 12126-12132, DOI: .

Supramolecular Self-Assembled Nanofibers Efficiently Activate the Precursor of Hepatocyte Growth Factor for Angiogenesis in Myocardial Infarction Therapy.

The reconstruction of blood perfusion is a crucial therapeutic method to save and protect cardiac function after acute myocardial infarction (AMI). The activation of the hepatocyte growth factor precursor (pro-HGF) has a significant effect on promoting angiogenesis and antiapoptosis. The oxygen/glucose deprivation (OGD) caused by AMI could induce vascular adventitia fibroblasts to differentiate into myofibroblasts and secrete the pro-HGF.

Dual-ligand supramolecular nanofibers inspired by the renin-angiotensin system for the targeting and synergistic therapy of myocardial infarction.

The compensatory activation of the renin-angiotensin system (RAS) after myocardial infarction (MI) plays a crucial role in the pathogenesis of heart failure. Most existing studies on this subject focus on mono- or dual-therapy of blocking the RAS, which exhibit limited efficacy and often causes serious adverse reactions. Few studies have been conducted on targeted therapy based on the activated RAS post-MI.

Enzyme-Instructed Self-Assembly Enabled Monomer-Excimer Transition to Construct Higher Ordered Luminescent Supramolecular Assembly for Activity-based Bioimaging.

It is challenging to construct high-performing excimer-based luminescent analytic tools at low molecular concentrations. We report that enzyme-instructed self-assembly (EISA) enables the monomer-excimer transition of a coumarin dye (Cou) at low molecular concentrations, and the resulting higher ordered luminescent supramolecular assemblies (i.e.

Furin-instructed molecular self-assembly actuates endoplasmic reticulum stress-mediated apoptosis for cancer therapy.

Protein quality control and proteostasis are essential to maintain cell survival as once disordered, they will trigger endoplasmic reticulum (ER) stress and even initiate apoptosis. Severe ER stress-mediated apoptosis is the cause of neurodegenerative diseases and expected to be a new target for cancer therapy. In this study, we designed a small molecule of 1-Nap to execute furin-instructed molecular self-assembly for selectively inhibiting the growth of MDA-MB-468 cells in vitro and in vivo.

Erratum: Ion Therapy: A Novel Strategy for Acute Myocardial Infarction.

[This corrects the article DOI: 10.1002/advs.201801260.

Dual-responsive self-assembly in lysosomes enables cell cycle arrest for locking glioma cell growth.

Herein we first report a dual-responsive peptide substrate (Comp. 1) for preparing self-assembled nanomaterials triggered by pH and legumain. The dual-responsive self-assembly of Comp.

IL-6-targeted ultrasmall superparamagnetic iron oxide nanoparticles for optimized MRI detection of atherosclerotic vulnerable plaques in rabbits.

Vulnerable plaques of atherosclerosis (AS) are the main culprit lesion for the serious risk of acute cardiovascular disease (CVD). Therefore, developing new non-invasive methods to detect vulnerable plaques and to evaluate their stability effectively is of great value in the early diagnosis of CVD. IL-6 plays a vital role in the development and rupture of AS.