{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T04:50:22Z","timestamp":1791521422986,"version":"4.3.4"},"reference-count":78,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T00:00:00Z","timestamp":1791504000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Mol. Biosci."],"abstract":"<jats:p>\n                    Heart failure (HF) is a complex systemic syndrome in which ongoing myocardial dysfunction and vascular alterations interact to drive disease progression. Given its pivotal role in cellular energetics and redox balance, nicotinamide adenine dinucleotide (NAD\n                    <jats:sup>+<\/jats:sup>\n                    ) has emerged as a key regulator of cardiovascular homeostasis. We recently demonstrated that myocardial NAD\n                    <jats:sup>+<\/jats:sup>\n                    depletion occurs early in Tg\u03b1q*44 mice, a model of chronic HF. Accordingly, this study sought to characterize systemic and vascular alterations in NAD\n                    <jats:sup>+<\/jats:sup>\n                    metabolism throughout the progression of HF by profiling circulating NAD\n                    <jats:sup>+<\/jats:sup>\n                    precursors and metabolites, and assessing vascular NAD\n                    <jats:sup>+<\/jats:sup>\n                    catabolic pattern. In female Tg\u03b1q*44 mice aged 4\u201314 months, whole-blood NAD\n                    <jats:sup>+<\/jats:sup>\n                    and serum nicotinamide (NAM) levels progressively declined with increasing HF severity and were strongly associated with deteriorating systolic function. Reduced circulating NAD\n                    <jats:sup>+<\/jats:sup>\n                    availability coincided with enhanced aortic NAD\n                    <jats:sup>+<\/jats:sup>\n                    turnover and increased aortic CD38 abundance in end-stage HF. In addition, we identified a low-molecular-weight VCAM-1-immunoreactive band in the aorta, consistent with enhanced vascular activation in Tg\u03b1q*44 mice. Advanced HF was also associated with perturbations in arginine-citrulline metabolism, characterized by elevated levels of methylated arginine derivatives that may compromise nitric oxide (NO) bioavailability. This was paralleled by progressive accumulation of 4-pyridone-3-carboxamide ribonucleoside (4PYR), an NAD\n                    <jats:sup>+<\/jats:sup>\n                    -derived endothelial toxin, whose levels correlated with all three methylarginines, suggesting convergent pathways of endothelial dysfunction. Collectively, these findings suggest that enhanced vascular NAD\n                    <jats:sup>+<\/jats:sup>\n                    catabolism, associated with increased CD38 abundance, constitutes a previously unrecognized metabolic feature of HF progression that may contribute to systemic NAD\n                    <jats:sup>+<\/jats:sup>\n                    dysregulation and endothelial dysfunction.\n                  <\/jats:p>","DOI":"10.3389\/fmolb.2026.1927197","type":"journal-article","created":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T04:26:15Z","timestamp":1791519975000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Circulating and vascular NAD+ metabolism remodeling in Tg\u03b1q*44 mice with progressive heart failure"],"prefix":"10.3389","volume":"13","author":[{"given":"Agata","family":"Jedrzejewska","sequence":"first","affiliation":[{"name":"Department of Biochemistry, Medical University of Gdansk","place":["Gdansk, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oliwia","family":"Krol","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Medical University of Gdansk","place":["Gdansk, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patryk","family":"Mucha","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Medical University of Gdansk","place":["Gdansk, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ada","family":"Kawecka","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Medical University of Gdansk","place":["Gdansk, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ewa","family":"Slominska","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Medical University of Gdansk","place":["Gdansk, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariola","family":"Olkowicz","sequence":"additional","affiliation":[{"name":"Department of Biopharmaceutics and Pharmacodynamics, Medical University of Gdansk","place":["Gdansk, Poland"]},{"name":"Jagiellonian Centre for Experimental Therapeutics (JCET), Jagiellonian University","place":["Krakow, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryszard T.","family":"Smolenski","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Medical University of Gdansk","place":["Gdansk, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marta","family":"Tomczyk","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Medical University of Gdansk","place":["Gdansk, Poland"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,10,9]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"11","DOI":"10.1016\/j.yjmcc.2022.01.008","article-title":"Benefits in cardiac function by CD38 suppression: improvement in NAD(+) levels, exercise capacity, heart rate variability and protection against catecholamine-induced ventricular arrhythmias","volume":"166","author":"Agorrody","year":"2022","journal-title":"J. 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