Peptides can be designed to self-assemble into predefined supramolecular nanostructures, which are then employed as biomaterials in a range of applications, including tissue engineering, drug delivery, and vaccination. However, current self-assembling peptide (SAP) hydrogels exhibit inadequate self-healing capacities and necessitate the use of sophisticated printing apparatus, rendering them unsuitable for 3D printing under physiological conditions. Here, we report a precisely designed charged peptide, Z5, with the object of investigating the impact of electrostatic interactions on the self-assembly and the rheological properties of the resulting hydrogels. This peptide displays salt-triggered self-assembly resulting in the formation of a nanofiber network with a high β-sheet content. The peptide self-assembly and the hydrogel properties can be modified according to the ionic environment. It is noteworthy that the Z5 hydrogel in normal saline (NS) shows exceptional self-healing properties, demonstrating the ability to recover its initial strength in seconds after the removal of shear force, thus rendering it an acceptable material for printing. In contrast, the strong salt shielding effect and the ionic cross-linking of Z5 hydrogels in PBS result in the bundling of peptide nanofibers, which impedes the recovery of the initial strength post-destruction. Furthermore, incorporating materials with varied charging properties into Z5 hydrogels can alter the electrostatic interactions among peptide nanofibers, further modulating the rheological properties and the printability of SAP hydrogels.

Background: Cardiovascular disease is associated with high morbidity and mortality. Doxorubicin (DOX) is an effective adjunct to cancer chemotherapy but leads to cardiovascular-related side effects. Because coenzyme Q10 (CoQ10) has been shown to protect against cardiac damage, this study was conducted to investigate the protective effects of CoQ10 against cardiac damage in mice. Methods: We randomly divided six-week-old male C57BL/6 mice into four groups: control (n = 7), CoQ10 (n = 7), heart failure (HF) (n = 7), and HF+CoQ10 (n = 6) groups. HF group was induced via intraperitoneal injections with DOX (5 mg/kg) once weekly for 4 weeks. CoQ10 was solube in corn oil. The mice of CoQ10 and HF+CoQ10 group were given CoQ10 (100 mg/kg) once a day for 8 weeks. All mice were subjected to different treatment regimens for eight weeks. Metabolic characteristics, cardiac damage, oxidative stress markers (SIRT1, SIRT3, eNOS, TE, P53, SIRT5, CAT, HO-1, and SOD), energy metabolism markers (PARP-1 and PPAR-γ), myocardial fibrosis markers (Smad3 and TGF-β), and apoptosis markers (BAK, BCL-XL, and caspase-8) were analyzed at eight weeks after the different treatments. Results: CoQ10 reduced the levels of molecules related to cardiac damage, oxidative stress, energy metabolism, and myocardial fibrosis in mice with doxorubicin-induced HF. CoQ10 also exerted anti-apoptotic effects in HF mice. Conclusions: CoQ10 may be useful for preventing cardiac damage in DOX-induced HF.

Pheochromocytomas are neuroendocrine tumors, and its cardiac involvement may include transient myocardial dysfunction, acute coronary syndrome (ACS), and even ventricular arrhythmias.A patient was referred for evaluation of stuttering chest pain, and his electrocardiogram showed T-wave inversion over leads V1 to V4. Coronary angiography showed 90% stenosis in the mid-left anterior descending coronary artery (LAD), which was stented. Five days later, the patient had ventricular tachycardia, and severe hypertension, remarkable blood pressure fluctuation between 224/76 and 70/50 mm Hg. The patient felt abdominal pain and his abdominal ultrasound showed suspicious right adrenal gland tumor. Enhanced computed tomography of adrenal gland conformed that there was a tumor in right adrenal gland accompanied by an upset level of aldosterone.The tumor was removed by laparoscope, and the pathological examination showed pheochromocytoma. After the surgery, the blood pressure turned normal gradually. There was no T-wave inversion in lead V1-V4. Our case illustrates a rare pheochromocytoma presentation with a VT and resembling ACS. In our case, the serious stenosis in the mid of LAD could be explained by worsen the clinical course of myocardial ischemia or severe coronary vasospasm by the excessive amounts of catecholamines released from the tumor. Coronary vasospasm was possible because he had no classic coronary risk factors (e.g. family history and smoking habit, essential hypertension, hyperglycemia and abnormal serum lipoprotein, high body mass index). Thus, pheochromocytoma was missed until he revealed the association of his symptoms with abdominalgia.As phaeochromocytomas that present with cardiovascular complications can be fatal, it is necessary to screen for the disease when patients present with symptoms indicating catecholamine excess.

The objective of this study is to investigate the sensitivity of contrast-enhanced transthoracic echocardiography (c-TTE) versus transesophageal echocardiography (TEE) to detect a residual right-to-left shunt (RLS) following a transcatheter patent foramen ovale (PFO) closure.A self-controlled study was conducted in a tertiary referral hospital. 57 patients with PFO who had experienced migraines underwent percutaneous PFO closure. c-TTE, TEE, and contrast-enhanced transcranial Doppler (c-TCD) at resting and Valsalva maneuver were performed during the 3-month follow-up after the closure.The closure devices were successfully implanted in all patients without complications. Three months after closure, TEE did not detect residual Valsalva shunts in any of the 57 patients; residual valsalva shunts were found via c-TTE in 15 of the 57 patients and were also observed via c-TCD. When c-TTE and/or c-TCD were used, the rate of residual RLSs detected in patients who underwent PFO closure was 26.32%, which was significantly different than the rate detected using TEE (P < .05)c-TTE and c-TCD showed equivalent sensitivity in evaluating transcatheter closure of a PFO. c-TTE could be a more cost-effective and reliable method to detect the residual shunt after PFO closure.

Background: Obesity can induce myocardial pyroptosis, but the exact mechanism is still unknown. A recent study reported the association of opa‐interacting protein 5‐antisense transcript 1 (OIP5‐AS1), an evolutionarily conserved long noncoding RNA, with pyroptosis. Therefore, this study aimed to investigate the role of OIP5‐AS1 in obesity‐induced myocardial pyroptosis.Methods: OIP5‐AS1 was downregulated in H9c2 cells, followed by treatment with 400 μM palmitic acid (PA). Propidium iodide (PI) staining, lactic dehydrogenase (LDH) release assay, caspase‐1 activity assay, IL‐1β, and IL‐18 activity assay were performed to detect pyroptotic phenotype. The interaction between OIP5‐AS1 and microRNAs (miRNAs) was analyzed using RNA pull‐down and luciferase assay. The effect of OIP5‐AS1 knockdown in high‐fat diet (HFD)‐induced obesity rat on cardiac function, myocardial hypertrophy, fibrosis, and remodeling was evaluated.Results: Fat deposition was observed in cardiomyocytes 24 h after PA treatment; moreover, PA‐treated cardiomyocytes showed significant increase in the rate of pyroptotic cells, release of LDH, protein expressions of NLRP3 and cleaved caspase‐1, and the activity of caspase‐1, IL‐1β, and IL‐18 as well as OIP5‐AS1 expression. These findings suggested that PA activated pyroptosis and induced OIP5‐AS1 expression in cardiomyocytes. Moreover, OIP5‐AS1 knockdown inhibited PA‐induced pyroptosis. Mechanistically, OIP5‐AS1 was found to specifically bind to miR‐22 and to regulate NLRP3 inflammasome‐mediated pyroptosis via miR‐22. Furthermore, OIP5‐AS1 knockdown ameliorated HFD‐induced cardiac dysfunction, myocardial hypertrophy, fibrosis, remodeling, and pyroptosis.Conclusion: Our results revealed that downregulation of OIP5‐AS1 can inhibit obesity‐induced myocardial pyroptosis via miR‐22/NLRP3 inflammasome axis. This finding lays a foundation of gene therapy for heart disease targeting OIP5‐AS1.

The long-term impact of left atrial appendage occlusion (LAAO) plus ablation for atrial fibrillation remains controversial. The present study aims to compare the three-year clinical outcomes of LAAO patients with or without one-staged ablation. The RECORD study (NCT03917563) was a prospective registry conducted in 39 participating sites in China between 1 April 2019 and 31 October 2020, which consecutively enrolled 3082 patients who successfully received the WATCHMAN LAAO device. The current study compared patients who received LAAO only to patients who underwent LAAO plus ablation. A 1:1 propensity score matching was performed to attenuate confounding. The primary outcome was a composite endpoint of cardiovascular death, stroke, and systemic embolism at 3-year. 1633/2928 (55.8%) patients received LAAO only and 1295/2928 (44.2%) received LAAO plus ablation. After propensity score matching, 1016/2032 (50.0%) were in the LAAO group and 1016/2032 (50.0%) in the LAAO plus ablation group. The mean ± SD age was 68.8 ± 9.3 years, with 815 (40.1%) participants being female. The mean ± SD CHA₂DS₂-VASc and HAS-BLED scores at baseline were 3.9 ± 1.8 and 2.4 ± 1.1, respectively. At three-year, compared to LAAO only, LAAO plus ablation was associated with a lower risk of cardiovascular death, stroke, systemic embolism (6.9%vs.10.4%, HR_PSM:0.66, 95%CI: 0.49–0.89, P = 0.007), which was driven mainly by the lower risk of cardiovascular death (3.7% vs. 7.3%, HR_PSM: 0.50, 95%CI: 0.34–0.74, P = 0.001). No significant between-group differences were noted for BARC-defined bleeding. LAAO plus ablation was associated with a lower risk of a composite of cardiovascular death, stroke, and systemic embolism than LAAO only at 3-year. However, given the observational nature of the current study, the results should be considered as hypothesis-generating only.