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Abstract Abdominal aortic aneurysms (AAA), with approximately 200,000 new diagnoses each year, represent a prevalent clinical concern. Current treatment includes monitoring and surgical procedures once the aneurysm reaches a certain size. However, the lack of effective, timely therapies leads to a high mortality rate due to rupture. With recent advancements and innovations in biomedical science, stem cell therapy has moved closer to widespread clinical use, with the field experiencing rapid growth since its inception in the late 20^thcentury. Given the pathophysiology of AAA, stem cell therapies have high potential impact in the treatment for both early and late-stage disease, targeting underlying mechanisms such as inflammation, vascular degeneration, and extracellular matrix degradation. There are many considerations and innovative potential approaches being explored in this type of treatment, such as strategically leveraging cell properties and their associated secretome and incorporating biomaterials-based strategies. This review article summarizes and critically assesses the efficacy of cell-based therapies in AAA preclinical models, current clinical trials in this area, and other emerging bioengineering approaches for the treatment of AAA. 

OBJECTIVETo characterize high type 1 diabetes (T1D) genetic risk in a population where type 2 diabetes (T2D) predominates. RESEARCH DESIGN AND METHODSCharacteristics typically associated with T1D were assessed in 109,594 Million Veteran Program participants with adult-onset diabetes, 2011–2021, who had T1D genetic risk scores (GRS) defined as low (0 to <45%), medium (45 to <90%), high (90 to <95%), or highest (≥95%). RESULTST1D characteristics increased progressively with higher genetic risk (P < 0.001 for trend). A GRS ≥ 90% was more common with diabetes diagnoses before age 40 years, but 95% of those participants were diagnosed at age ≥40 years, and they resembled T2D in mean age (64.3 years) and BMI (32.3 kg/m2). Compared with the low risk group, the highest-risk group was more likely to have diabetic ketoacidosis (low 0.9% vs. highest GRS 3.7%), hypoglycemia prompting emergency visits (3.7% vs. 5.8%), outpatient plasma glucose <50 mg/dL (7.5% vs. 13.4%), a shorter median time to start insulin (3.5 vs. 1.4 years), use of a T1D diagnostic code (16.3% vs. 28.1%), low C-peptide levels if tested (1.8% vs. 32.4%), and glutamic acid decarboxylase antibodies (6.9% vs. 45.2%), all P < 0.001. CONCLUSIONSCharacteristics associated with T1D were increased with higher genetic risk, and especially with the top 10% of risk. However, the age and BMI of those participants resemble people with T2D, and a substantial proportion did not have diagnostic testing or use of T1D diagnostic codes. T1D genetic screening could be used to aid identification of adult-onset T1D in settings in which T2D predominates.