Acute myocardial infarction (AMI) results in weakening of the heart muscle and an increased risk for chronic heart failure. Therapeutic stem cells have been shown to reduce inflammatory signaling and scar tissue expansion, despite most of these studies being limited by poor retention of cells. Gelatin methacrylate (GelMA) coatings have been shown to increase the retention of these therapeutic cells near the infarct. In this work, we evaluate two different potential binding partners for GelMA-coated bone marrow cells (BMCs) and myocardial tissue: the extracellular matrix (ECM) and interstitial non-cardiomyocytes. While cells containing β1 integrins mediate cell-ECM adhesion in vivo, these cells do not promote binding to our collagen-degraded, GelMA coating. Specifically, microscopic imagining shows that even with high integrin expression, GelMA-coated BMCs do not bind to cells within the myocardium. Alternatively, BMC incubation with decellularized heart tissue results in higher adhesion of coated cells versus uncoated cells supporting our GelMA-ECM binding mode. To further evaluate the ECM binding mode, cells were incubated on slides modified with one of three different major heart ECM components: collagen, laminin, or fibronectin. While all three components promoted higher adhesion than unmodified glass, collagen-coated slides resulted in a significantly higher adhesion of GelMA-coated BMCs over laminin and fibronectin. Incubation with unmodified BMCs confirmed that without a GelMA coating minimal adhesion of BMCs occurred. We conclude that GelMA cellular coatings significantly increase the binding of cells to collagen within the ECM. Our results provide progress towards a biocompatible and easily translatable method to enhance the retention of transplanted cells in human studies.

Bortezomib is a 26S proteasome inhibitor used to treat multiple myeloma and systemic amyloidosis. While effective in prolonging survival, bortezomib has been increasingly associated with cardiovascular adverse events (CVAEs), such as cardiac failure and arrhythmias. However, a comprehensive post-marketing safety profile has not been fully established. We analyzed cardiovascular adverse events reported between May 2003 and May 2025 using the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS) via the Open Vigil 2.1 platform. Disproportionality analysis was conducted using the reporting odds ratio (ROR) with 95% confidence intervals (CI) to detect statistically significant adverse reports. Of over 9 million drug-related adverse events in the FAERS database, 552 Cardiac events were linked to bortezomib. Cardiac amyloidosis showed the strongest association (ROR: 35.58; 95% CI: 28.16–44.95), followed by atrial flutter (ROR: 4.34; 95% CI: 3.41–5.52), left ventricular dysfunction (ROR: 4.25; 95% CI: 3.26–5.55), cardiac failure, acute (ROR: 3.66; 95% CI: 2.75–4.86), congestive cardiomyopathy (ROR: 3.23; 95% CI: 2.33–4.49), hypertrophic cardiomyopathy (ROR: 3.44; 95% CI: 1.95–6.08), cardiac failure (ROR: 3.18; 95% CI: 2.93–3.46), cardiomyopathy (ROR: 2.81; 95% CI: 2.30–3.43), atrial fibrillation (ROR: 2.65; 95% CI: 2.43–2.89), right ventricular failure (ROR: 2.30; 95% CI: 1.63–3.24), myocarditis (ROR: 2.25; 95% CI: 1.73–2.91), and supraventricular tachycardia (ROR: 2.17; 95% CI: 1.61–2.93). cardiac failure led to the highest number of hospitalizations (301) and deaths (208), followed by atrial fibrillation and cardiac amyloidosis. Older adults (≥65 years) and patients with amyloidosis or myeloma were the most vulnerable groups. Bortezomib is associated with a wide spectrum of serious cardiac adverse events, with cardiac amyloidosis and cardiac failure demonstrating particularly high disproportionality and mortality. These findings emphasize the need for routine cardiovascular risk assessment and proactive monitoring in high-risk patient populations receiving bortezomib.

Bortezomib is a 26S proteasome inhibitor used to treat multiple myeloma and systemic amyloidosis. While effective in prolonging survival, bortezomib has been increasingly associated with cardiovascular adverse events (CVAEs), including cardiac failure and arrhythmias, yet a comprehensive post-marketing cardiac safety profile remains incompletely defined. We analyzed cardiovascular adverse events reported between May 2003 and May 2025 using the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS) via the OpenVigil 2.1 platform. Disproportionality analysis was performed using reporting odds ratios (RORs) with 95% confidence intervals (CIs). Among over 9 million drug-related adverse events in FAERS, 552 cardiac events were linked to bortezomib. Several cardiac outcomes, including atrial flutter, left ventricular dysfunction, cardiac failure, cardiomyopathy, atrial fibrillation, right ventricular failure, myocarditis, and supraventricular tachycardia, demonstrated elevated disproportionality signals. Separately, cardiac amyloidosis exhibited the highest disproportionality signal (ROR: 35.58; 95% CI: 28.16–44.95), a finding that reflects underlying disease severity rather than treatment-emergent cardiotoxicity. Cardiac failure accounted for the greatest number of hospitalizations (301) and deaths (208), followed by atrial fibrillation and cardiac amyloidosis. Older adults (≥65 years) and patients with amyloidosis or multiple myeloma were the most vulnerable populations. Overall, bortezomib was associated with serious cardiac adverse events, particularly cardiac failure and atrial arrhythmias, underscoring the need for routine cardiovascular risk assessment and proactive monitoring in high-risk patients.