The roles of Th cells in myocardial infarction.

Myocardial infarction, commonly known as a heart attack, is a serious condition caused by the abrupt stoppage of blood flow to a part of the heart, leading to tissue damage. A significant aspect of this condition is reperfusion injury, which occurs when blood flow is restored but exacerbates the damage. This review first addresses the role of the innate immune system, including neutrophils and macrophages, in the cascade of events leading to myocardial infarction and reperfusion injury.

Classification of regulatory T cells and their role in myocardial ischemia-reperfusion injury.

Myocardial ischemia-reperfusion injury (MIRI) is closely related to the final infarct size in acute myocardial infarction (AMI). Therefore, reducing MIRI can effectively improve the prognosis of AMI patients. At the same time, the healing process after AMI is closely related to the local inflammatory microenvironment.

Application of locally responsive design of biomaterials based on microenvironmental changes in myocardial infarction.

Morbidity and mortality caused by acute myocardial infarction (AMI) are on the rise, posing a grave threat to the health of the general population. Up to now, interventional, surgical, and pharmaceutical therapies have been the main treatment methods for AMI. Effective and timely reperfusion therapy decreases mortality, but it cannot stimulate myocardial cell regeneration or reverse ventricular remodeling.

A pH/H O /MMP9 Time-Response Gel System with Sparc Tregs Derived Extracellular Vesicles Promote Recovery After Acute Myocardial Infarction.

Regulatory T cells overexpressing SPARC (secreted protein acidic and cysteine rich) (Sparc Tregs) can help repair infarct tissues after acute myocardial infarction (AMI). This research demonstrates that Sparc Treg-derived extracellular vesicles (EVs) effectively improved cardiac function through proinflammatory factors IL-1β, IL-6, and TNF-α inhibition and collagen synthesis related gene Col3a1 promotion in AMI; moreover, a composite hydrogel-EVs system (DHPM(4APPC)_EVs) is designed based on Sparc Treg-derived EVs with CXCR2 overexpressing and pH/H O /MMP9 temporally responsive gel microspheres. In AMI, due to the levels of chemokine, pH, H O , and MMP9 enzymes in the infarct area, DHPM(4APPC)_EVs can effectively target the infarct area, release the loaded EVs, form the gel to capture the released EVs, and slowly release the captured EVs, contribute to promote EVs to stay in the infarct area for a long time to play the repair function, so as to reduce myocardial injury and promote the improvement of cardiac function.

Gelation of highly entangled hydrophobic macromolecular fluid for ultrastrong underwater in situ fast tissue adhesion.

Although strong underwater bioadhesion is important for many biomedical applications, designing adhesives to perform in the presence of body fluids proves to be a challenge. To address this, we propose an underwater and in situ applicable hydrophobic adhesive (UIHA) composed of polydimethylsiloxane, entangled macromolecular silicone fluid, and a reactive silane. The hydrophobic fluid displaced the boundary water, formed an in situ gel, bonded to tissues, and achieved exceptional underwater adhesion strength.

Targeted Intervention of NF2-YAP Signaling Axis in CD24-Overexpressing Cells Contributes to Encouraging Therapeutic Effects in TNBC.

Triple-negative breast cancer (TNBC) cells have not been usefully classified, and no targeted therapeutic plans are currently available, resulting in a high recurrence rate and metastasis potential. In this research, CD24 cells accounted for the vast majority of TNBC cells, and they were insensitive to Taxol but sensitive to ferroptosis agonists and effectively escaped phagocytosis by tumor-associated macrophages. Furthermore, the NF2-YAP signaling axis modulated the expression of ferroptosis suppressor protein 1 (FSP1) and CD24 in CD24 cells, with subsequent ferroptotic regulation and macrophage phagocytosis.

Amelioration of acute myocardial infarction injury through targeted ferritin nanocages loaded with an ALKBH5 inhibitor.

The roles of mA RNA methylation and mitochondrial metabolism in acute myocardial infarction (AMI) remain unclear. In this study, we demonstrated that mA RNA methylation affected ischemia/reperfusion (I/R) injury in AMI through the "Erasers" protein ALKBH5-related metabolic reprogramming, characterized by the inhibition of enzyme activities of the tricarboxylic acid cycle; moreover, a surface-modified bioengineered ferritin nanocage was obtained from Archaeoglobus fulgidus, with a chimeric structure containing 8 lysine residues, SpyTag/SpyCatcher, and the C1q ligand Scarf1, which could disassemble and self-assemble in neutral solutions according to different Mg concentrations. The surface-modified bioengineered ferritin nanocage targeted the dying cells in the infarct area under the guidance of Scarf1.

Precisely and Efficiently Enzyme Response Microspheres with Immune Removal Escape Loaded with MCC950 Ameliorate Cardiac Dysfunction in Acute Myocardial Infarction.

Although the percutaneous coronary intervention (PCI)treatment can improve the survival rate of acute myocardial infarction (AMI) patients, the early granulocytes response within 6 hours can induce second injuries during the reperfusion process. The new drug delivery system MMP9 hydrolytic microspheres (NMM) with negatively charged surface was designed out and MCC950 (MCC) was loaded into NMM (NMM-M), MCC is the inhibitor of nucleotide binding oligomerization domain (NOD)-like receptor, pyrin containing domain 3 (NLRP3)-inflammasome which is the key promoter of granulocytes-induced injury. NMM-M could effectively escape the phagocytosis of immune phagocytes in the blood, and target the ischemic region based on the electrostatic attraction and the attraction of enzyme to substrate, and sudden release the loaded MCC within 2 hours.

A novel dressing seeded with embryonic artery CD133 cells and loaded with the Sirt1 agonist SRT1720 accelerates the healing of diabetic ischemic ulcers.

Refractory ischemic ulcers that occur in patients with diabetes present a major clinical challenge. Embryonic artery cluster of differentiation 133 cells (EACCs) may promote the healing of diabetic ulcers; however, the high glucose environment in the diabetic ulcers decreases the survival rate of transplanted EACCs and inhibit their biological function. Furthermore, microcirculation in diabetic ischemic ulcers is impaired, which inhibits the beneficial effect of EACCs.

Rapid Delivery of Hsa-miR-590-3p Using Targeted Exosomes to Treat Acute Myocardial Infarction Through Regulation of the Cell Cycle.

Acute myocardial infarction leads to heart failure due to inadequate regeneration of cardiomyocytes. Therefore, promotion of cardiomyocyte proliferation is the key for the restoration of cardiac function. Induction of the cell cycle and the downregulation of genes that inhibit cardiomyocyte proliferation could induce cardiomyocyte to re-enter into the proliferative state.

An inflammatory memory and angiogenic self-assembling nanofiber hydrogel scaffold seeded with to accelerate the healing of diabetic ischemic ulcers.

Refractory ulcers are a major challenge in the treatment of a diabetic foot, because of the immunodeficient, ischemic and high-glucose microenvironment. Inflammatory memory peptides, which were extracted from the immune mediator absent in melanoma 2 (AIM2), could effectively improve the immunodeficient microenvironment and special angiogenic peptides could effectively promote angiogenesis. Moreover, the gut flora () participates in diabetic metabolism and could decrease high-glucose levels.

A VEGF delivery system targeting MI improves angiogenesis and cardiac function based on the tropism of MSCs and layer-by-layer self-assembly.

Myocardial infarction (MI) is a serious ischemic condition affecting many individuals around the world. Vascular endothelial growth factor (VEGF) is considered a promising factor for enhancing cardiac function by promoting angiogenesis. However, the lack of a suitable method of VEGF delivery to the MI area is a serious challenge.

PLGA-PNIPAM Microspheres Loaded with the Gastrointestinal Nutrient NaB Ameliorate Cardiac Dysfunction by Activating Sirt3 in Acute Myocardial Infarction.

Acute myocardial infarction (AMI) is the death of cardiomyocytes caused by a lack of energy due to ischemia. Nutrients supplied by the blood are the main source of cellular energy for cardiomyocytes. Sodium butyrate (NaB), a gastrointestinal nutrient, is a short-chain fatty acid (butyric acid) that may act as an energy source in AMI therapy.

AU4S: a novel synthetic peptide to measure the activity of ATG4 in living cells.

ATG4 plays a key role in autophagy induction, but the methods for monitoring ATG4 activity in living cells are limited. Here we designed a novel fluorescent peptide named AU4S for noninvasive detection of ATG4 activity in living cells, which consists of the cell-penetrating peptide (CPP), ATG4-recognized sequence "GTFG," and the fluorophore FITC. Additionally, an ATG4-resistant peptide AG4R was used as a control.

Natural Bcl-2 inhibitor (-)- gossypol induces protective autophagy via reactive oxygen species-high mobility group box 1 pathway in Burkitt lymphoma.

(-)- Gossypol, a natural inhibitor of anti-apoptotic Bcl-2 proteins, has presented an effective anti-tumor activity in numerous preclinical trials. More and more evidence in vivo and in vitro validates that (-)- gossypol can dramatically suppress cell proliferation and induce cell death in hematological malignancies. However, the detailed mechanisms are not well known.