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(Landmark Ed)"],"abstract":"<jats:p>Background: Inflammation plays a pivotal role in the progression of tissue fibrosis. Our previous research demonstrated that Na+, K+-ATPase (NKA) \u03b11 deficiency impairs mitochondrial function and accelerates isoproterenol (ISO)-induced cardiac remodeling. This study aims to investigate the interplay between inflammation and NKA\u03b11 deficiency in ISO-induced cardiac fibrosis. Methods: Age-matched male wild-type (WT) and NKA\u03b11+\/- mice received daily subcutaneous injections of ISO (30 mg\/kg body weight) over 14 consecutive days. Comprehensive histopathological evaluation was performed to assess myocardial architecture and leukocyte infiltration profiles. Mitochondrial ultrastructure was analyzed using transmission electron microscopy. The molecular techniques of real-time quantitative polymerase chain reaction (RT-qPCR), immunoblotting, and enzyme-linked immunosorbent assay (ELISA) were utilized to quantify fibrotic markers and inflammatory mediators. A cell co-culture model was established to investigate the interactions between different cell types. Results: NKA\u03b11 haploinsufficiency exacerbated heart lesions and fibrosis, led to macrophage accumulation, and increased the expression of inflammatory factors in ISO-challenged hearts. Although NKA\u03b11 deficiency did not directly activate macrophages or fibroblasts under ISO conditions, it significantly accelerated cardiomyocyte death in response to ISO insult. Paracrine crosstalk between damaged NKA\u03b11+\/- cardiomyocytes, macrophages, and fibroblasts amplified macrophage activation, inflammatory cytokine release, and fibroblast differentiation. Estrogen-related receptor \u03b1 (ERR\u03b1) was identified as a key mediator of NKA\u03b11 haploinsufficiency-induced cardiomyocyte death and interleukin-18 (IL-18) release. Furthermore, treatment with an NKA\u03b11 897DVEDSYGQQWTYEQR911 (DR)-region antibody mitigated ISO-induced cardiac fibrosis and macrophage infiltration. Conclusion: This study provides evidence that NKA\u03b11 deficiency exacerbates cardiac fibrosis by promoting ERR\u03b1-dependent cardiomyocyte death and by facilitating intercellular cross-talk between damaged NKA\u03b11+\/- cardiomyocytes, macrophages, and fibroblasts. Based on these findings, we suggest that NKA\u03b11 may be a potential regulator of cardiac fibrosis, and that its DR-region represents a potential therapeutic target.<\/jats:p>","DOI":"10.31083\/fbl40363","type":"journal-article","created":{"date-parts":[[2025,8,6]],"date-time":"2025-08-06T06:16:39Z","timestamp":1754460999000},"source":"Crossref","is-referenced-by-count":0,"title":["Na+,-K+-ATPase Deficiency Exacerbates Cardiac Fibrosis via Promoting ERR\u03b1-Mediated Myocardial Cell Injury and Macrophage Activation Under Isoproterenol-Challenged Conditions"],"prefix":"10.31083","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0009-0000-5657-5004","authenticated-orcid":true,"given":"Ting","family":"Lei","sequence":"first","affiliation":[{"name":"Department of Clinical Laboratory, Xi\u2019an People\u2019s Hospital (Xi\u2019an Fourth Hospital), 710004 Xi\u2019an, Shaanxi, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-7294-8274","authenticated-orcid":true,"given":"Tao","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Clinical Laboratory, Xi\u2019an People\u2019s Hospital (Xi\u2019an Fourth Hospital), 710004 Xi\u2019an, Shaanxi, China"},{"name":"Department of Biochemistry and Molecular Biology, Xi\u2019an Jiaotong University, 710061 Xi\u2019an, Shaanxi, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-6973-4842","authenticated-orcid":true,"given":"Yutong","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Xi\u2019an Jiaotong University, 710061 Xi\u2019an, Shaanxi, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-3793-0052","authenticated-orcid":true,"given":"Yingnan","family":"Zhai","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Xi\u2019an Jiaotong University, 710061 Xi\u2019an, Shaanxi, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-6682-6255","authenticated-orcid":true,"given":"Ruijia","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Xi\u2019an Jiaotong University, 710061 Xi\u2019an, Shaanxi, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-4259-337X","authenticated-orcid":true,"given":"Xiaoyi","family":"Tan","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Xi\u2019an Jiaotong University, 710061 Xi\u2019an, Shaanxi, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3479-3315","authenticated-orcid":true,"given":"Hongli","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Clinical Laboratory, Xi\u2019an People\u2019s Hospital (Xi\u2019an Fourth Hospital), 710004 Xi\u2019an, Shaanxi, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5654-7206","authenticated-orcid":true,"given":"Xiaofei","family":"Yan","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology, Xi\u2019an Jiaotong University, 710061 Xi\u2019an, Shaanxi, China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"16242","published-online":{"date-parts":[[2025,7,29]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","unstructured":"Ravassa S, L\u00f3pez B, Treibel TA, San Jos\u00e9 G, Losada-Fuentenebro B, Tapia L, et al. 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