Publications

Cardiac fibrosis and remodeling are critical contributors to heart failure, particularly in the context of diabetes, where hyperglycemia (HG) exacerbates pathological fibroblast activity. Despite the known cardiovascular benefits of canagliflozin (CANA), its specific effects on human cardiac fibroblasts (HCFs) under HG conditions remain unexplored. We investigated whether CANA could mitigate HG-induced detrimental responses in HCFs. Dose-response assays revealed that 100 nM CANA significantly reduced HG-induced proliferation and migration of HCFs. Furthermore, CANA attenuated mitochondrial reactive oxygen species (ROS) production, a key driver of myofibroblast differentiation, and suppressed HG-induced expression of SMAD2, a critical activator of cardiac fibroblasts. Additionally, HG disrupted calcium (Ca2+) homeostasis, which was ameliorated by CANA treatment. These findings collectively demonstrate that CANA exerts protective effects on HCFs by improving mitochondrial function, restoring Ca2+ handling, and reducing fibroblast proliferation, migration, and activation under HG conditions.

Prevention of dementia represents a public health priority. Hypertension is a risk factor for mild cognitive impairment (MCI), a precursor to progressive dementia. A great effort is underway to develop accurate and sensitive tools to detect the MCI condition in hypertensive patients. To investigate the potential association of subclinical left ventricular dysfunction expressed by the global longitudinal strain (GLS) with the MCI, defined by the Italian version of the quick mild cognitive impairment (Qmci-I). This multi-centric study included 180 consecutive hypertensive patients without medical diseases and/or drugs with known significant effects on cognition but with a not negligible comorbidity burden to avoid a possible "hyper-normality bias". The study cohort was classified into two main groups concerning the median value of the GLS. A weighted logistic regression model was employed after an inverse probability of treatment weighting (IPTW) analysis to characterize a potential association between GLS and MCI. Almost 41,1% of the whole study population was female. The mean age was 65,6 ± 7,2. 39 patients (21,7%) showed MCI. After IPTW, the GLS was significantly associated with the study endpoint (OR, 1,22; 95% CI: 1,07-1,39, P = 0.003). Our results highlight that the GLS is a potential predictor of MCI and, therefore, a valuable tool for establishing preventive strategies to arrest the progression toward a cognitive decline in hypertensive patients.

OBJECTIVE: This article presents the design, development, and implementation of a novel and innovative virtual reality (VR) simulation aimed at increasing nursing skills in identifying, managing, and deescalating workplace violence (WPV) incidents and mitigating the effects after critical incidents.

BACKGROUND: The ANA reports that 1 in 4 nurses in the United States experience workplace assault annually, highlighting the novel role of VR simulations in educating and preparing nurses to recognize, address, and minimize the impact of WPV.

METHODS: A multidisciplinary team designed and implemented a VR simulation based on real WPV incidents reported by nurses in an urban health system, enlisting a film and video company's expertise to bring scenarios to life, addressing a critical gap.

CONCLUSIONS: This article discusses the collaborative creation of simulations using VR as a novel strategy for educating nurses on identification, management, and deescalation of incidents of WPV and mitigating the effects of WPV after critical incidents.

Mitochondria serve an essential metabolic and energetic role in cellular activity, and their dysfunction has been implicated in a wide range of disorders, including cardiovascular conditions, neurodegenerative disorders, and metabolic syndromes. Mitochondria-targeted therapies, such as Elamipretide (SS-31, MTP-131, Bendavia), have consequently emerged as a topic of scientific and clinical interest. Elamipretide has a unique structure allowing for uptake in a variety of cell types and highly selective mitochondrial targeting. This mitochondria-targeting tetrapeptide selectively binds cardiolipin (CL), a lipid found in the inner mitochondrial membrane, thus stabilizing mitochondrial cristae structure, reducing oxidative stress, and enhancing adenosine triphosphate (ATP) production. Preclinical studies have demonstrated the protective and restorative efficacy of Elamipretide in models of heart failure, neurodegeneration, ischemia-reperfusion injury, metabolic syndromes, and muscle atrophy and weakness. Clinical trials such as PROGRESS-HF, TAZPOWER, MMPOWER-3, and ReCLAIM elaborate on preclinical findings and highlight the significant therapeutic potential of Elamipretide. Further research may expand its application to other diseases involving mitochondrial dysfunction as well as investigate long-term efficacy and safety of the drug. The following review synthesizes current knowledge of the structure, mechanisms of action, and the promising therapeutic role of Elamipretide in stabilizing mitochondrial fitness, improving mitochondrial bioenergetics, and minimizing oxidative stress.