{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T16:24:09Z","timestamp":1791563049136,"version":"4.3.4"},"reference-count":60,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2021,10,7]],"date-time":"2021-10-07T00:00:00Z","timestamp":1633564800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004281","name":"National Science Centre","doi-asserted-by":"publisher","award":["UMO 2018\/29\/N\/NZ24\/02915"],"award-info":[{"award-number":["UMO 2018\/29\/N\/NZ24\/02915"]}],"id":[{"id":"10.13039\/501100004281","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Team Tech\u2013Core Facility program of the FNP"},{"name":"European Union under the European Regional Development Fund","award":["OPUS 12 grant (no. UMO 2016\/23\/B\/ST4\/00795 to K.M.M.)"],"award-info":[{"award-number":["OPUS 12 grant (no. UMO 2016\/23\/B\/ST4\/00795 to K.M.M.)"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,9,20]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Endothelial dysfunction (ED) and red blood cell distribution width (RDW) are both prognostic factors in heart failure (HF), but the relationship between them is not clear. In this study, we used a unique mouse model of chronic HF driven by cardiomyocyte-specific overexpression of activated G\u03b1q protein (Tg\u03b1q*44 mice) to characterize the relationship between the development of peripheral ED and the occurrence of structural nanomechanical and biochemical changes in red blood cells (RBCs).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>Systemic ED was detected in vivo in 8-month-old Tg\u03b1q*44 mice, as evidenced by impaired acetylcholine-induced vasodilation in the aorta and increased endothelial permeability in the brachiocephalic artery. ED in the aorta was associated with impaired nitric oxide (NO) production in the aorta and diminished systemic NO bioavailability. ED in the aorta was also characterized by increased superoxide and eicosanoid production. In 4- to 6-month-old Tg\u03b1q*44 mice, RBC size and membrane composition displayed alterations that did not result in significant changes in their nanomechanical and functional properties. However, 8-month-old Tg\u03b1q*44 mice presented greatly accentuated structural and size changes and increased RBC stiffness. In 12-month-old Tg\u03b1q*44 mice, the erythropathy was featured by severely altered RBC shape and elasticity, increased RDW, impaired RBC deformability, and increased oxidative stress (gluthatione (GSH)\/glutathione disulfide (GSSG) ratio). Moreover, RBCs taken from 12-month-old Tg\u03b1q*44 mice, but not from 12-month-old FVB mice, coincubated with aortic rings from FVB mice, induced impaired endothelium-dependent vasodilation and this effect was partially reversed by an arginase inhibitor [2(S)-amino-6-boronohexanoic acid].<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>In the Tg\u03b1q*44 murine model of HF, systemic ED accelerates erythropathy and, conversely, erythropathy may contribute to ED. These results suggest that erythropathy may be regarded as a marker and a mediator of systemic ED in HF. RBC arginase and possibly other RBC-mediated mechanisms may represent novel therapeutic targets for systemic ED in HF.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/cvr\/cvab306","type":"journal-article","created":{"date-parts":[[2021,10,6]],"date-time":"2021-10-06T09:05:43Z","timestamp":1633511143000},"page":"2610-2624","source":"Crossref","is-referenced-by-count":42,"title":["Temporal relationship between systemic endothelial dysfunction and alterations in erythrocyte function in a murine model of chronic heart failure"],"prefix":"10.1093","volume":"118","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7495-3945","authenticated-orcid":false,"given":"Tasnim","family":"Mohaissen","sequence":"first","affiliation":[{"name":"Jagiellonian University, Jagiellonian Center for Experimental Therapeutics (JCET) , 14 Bobrzynskiego St., 30-348 Krakow , Poland"},{"name":"Jagiellonian University Medical College, Faculty of Pharmacy , 9 Medyczna St., 30-688, Krakow , 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