{"entity": "researcher", "timestamp": "2026-09-23T21:35:51.315Z", "family": "B\u00e4ck", "given": "Magnus", "initials": "M", "orcid": "0000-0003-0853-5141", "affiliations": ["Department of Medicine Solna, Karolinska Institutet and Department of Cardiology, Karolinska University Hospital Stockholm, Sweden (O.P., S.-C.P., M.B.)."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/16eee4e6ca81489389f2c87675a66922.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/16eee4e6ca81489389f2c87675a66922"}}, "publications": [{"entity": "publication", "iuid": "2cd2ab509ab146019309ec9452cfb70d", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/2cd2ab509ab146019309ec9452cfb70d.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/2cd2ab509ab146019309ec9452cfb70d"}}, "title": "Advances in single-cell transcriptomics: unraveling the pathogenesis of calcific aortic valve disease.", "authors": [{"family": "Qin", "given": "Zihan", "initials": "Z", "orcid": "0000-0002-2380-6096", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/cadc22178b96449789bee8adf4c91944.json"}}, {"family": "B\u00e4ck", "given": "Magnus", "initials": "M", "orcid": "0000-0003-0853-5141", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/16eee4e6ca81489389f2c87675a66922.json"}}], "type": "journal article", "published": "2026-02-14", "journal": {"title": "Cardiovasc Res", "issn": "1755-3245", "volume": "121", "issue": "18", "pages": "2838-2859", "issn-l": null}, "abstract": "Single-cell RNA sequencing (scRNA-seq) has revolutionized the study of calcified aortic valve disease (CAVD) by enabling the dissection of cellular heterogeneity, lineage differentiation, and intercellular crosstalk at an unprecedented resolution. It revealed original vistas into the mechanisms of CAVD and novel putative therapeutic targets. This review provides a narrative state-of-the-art overview of scRNA-seq applications in CAVD research, summarizing key findings on valvular cell populations, disease-associated phenotypic transitions, and molecular pathways driving pathological remodeling. Additionally, the translational potential of single-cell technologies in identifying novel therapeutic targets is discussed, as well as the current challenges and future directions in this rapidly evolving field.", "doi": "10.1093/cvr/cvaf255", "pmid": "41264422", "labels": [], "xrefs": [{"db": "pii", "key": "8331986"}], "notes": [], "created": "2026-09-23T11:37:34.483Z", "modified": "2026-09-23T11:37:34.606Z"}, {"entity": "publication", "iuid": "0359da20e6424ed89b9bd311fa0ef67b", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/0359da20e6424ed89b9bd311fa0ef67b.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/0359da20e6424ed89b9bd311fa0ef67b"}}, "title": "Vascular Bed-Specific Endothelial Dysfunction and Age-Dependent Circadian Hypertension in Mice Lacking the Resolvin D2 Receptor GPR18.", "authors": [{"family": "de Moudt", "given": "Sofie", "initials": "S"}, {"family": "Sitek", "given": "Barbara", "initials": "B"}, {"family": "Bar", "given": "Anna", "initials": "A"}, {"family": "Lourenco-Rodrigues", "given": "Marc-Damien", "initials": "MD"}, {"family": "Lagrange", "given": "J\u00e9r\u00e9my", "initials": "J"}, {"family": "Yen", "given": "Frances T", "initials": "FT"}, {"family": "Ch\u0142opicki", "given": "Stefan", "initials": "S", "orcid": "0000-0002-2878-3858", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/96d560123c51471aa8ee9ef21521a39f.json"}}, {"family": "Mercier", "given": "Nathalie", "initials": "N"}, {"family": "B\u00e4ck", "given": "Magnus", "initials": "M", "orcid": "0000-0003-0853-5141", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/16eee4e6ca81489389f2c87675a66922.json"}}], "type": "journal article", "published": "2025-12-15", "journal": {"title": "FASEB J.", "issn": "1530-6860", "volume": "39", "issue": "23", "pages": "e71245", "issn-l": "0892-6638"}, "abstract": "G protein-coupled receptor (GPR) 18 is the receptor for the specialized pro-resolving lipid mediator (SPM) RvD2, which has proven efficacy in preventing atherosclerosis in mice. The aim of the present study was to establish direct vascular effects of GPR18 signaling. GPR18 knockout (KO) and wildtype (WT) mice underwent magnetic resonance imaging (MRI) for in vivo determination of endothelial function, and continuous 24 h telemetry for in vivo blood pressure monitoring. Isolated vessels derived from GPR18 KO and wildtype mice were used for determinations of ex vivo vascular reactivity and immunofluorescent quantifications. GPR18 KO mice exhibited endothelial dysfunction in the femoral arterial segment measured by MRI in vivo and in isolated arteries ex vivo as impaired ACh-induced vasodilatation, whereas the sensitivity to exogenous NO was unchanged. Endothelial function was not significantly different in the thoracic aortic segment between GPR18 KO and WT mice, demonstrating vascular bed-specific endothelial dysfunction as a result of GPR18 deletion. A significantly reduced eNOS expression and a larger indomethacin-sensitive component in ACh-induced relaxations observed in femoral arteries derived from GPR18 KO compared with WT mice suggest that the dysfunctional eNOS-mediated femoral endothelial function may be partly compensated by increased relaxant prostanoid modulation. Finally, conscious mean arterial blood pressure recorded by telemetry was significantly higher daytime compared with wildtype mice at 24 h telemetry measures, whereas young mice did not exhibit any significant differences in day- and night-time blood pressure. These observations linking GPR18 to vascular bed-specific endothelial dysfunction and age-dependent hypertension point to beneficial pro-resolving cardiovascular effects through GPR18 during aging.", "doi": "10.1096/fj.202503386R", "pmid": "41324396", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC12668024"}], "notes": [], "created": "2026-09-23T12:36:23.825Z", "modified": "2026-09-23T12:36:23.935Z"}, {"entity": "publication", "iuid": "0951c58772bd41b781834734a97e7d48", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/0951c58772bd41b781834734a97e7d48.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/0951c58772bd41b781834734a97e7d48"}}, "title": "Decoding the ankle-brachial index in peripheral artery disease: coronary versus valvular calcification.", "authors": [{"family": "Petri", "given": "Marcelo Heron", "initials": "MH", "orcid": "0000-0002-6892-2680", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1f6f650422504a90ade4a97798e88460.json"}}, {"family": "Haftbaradaran Esfahani", "given": "Payam", "initials": "P"}, {"family": "Plunde", "given": "Oscar", "initials": "O", "orcid": "0000-0003-1343-2198", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/119743fc4a1d46029dd0dd10921464ca.json"}}, {"family": "B\u00e4ck", "given": "Magnus", "initials": "M", "orcid": "0000-0003-0853-5141", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/16eee4e6ca81489389f2c87675a66922.json"}}], "type": "editorial", "published": "2025-11-00", "journal": {"title": "Eur Heart J Open", "issn": "2752-4191", "volume": "5", "issue": "6", "pages": "oeaf134", "issn-l": null}, "abstract": null, "doi": "10.1093/ehjopen/oeaf134", "pmid": "41377092", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC12686984"}, {"db": "pii", "key": "oeaf134"}], "notes": [], "created": "2026-09-23T14:54:31.381Z", "modified": "2026-09-23T14:54:31.530Z"}, {"entity": "publication", "iuid": "f5802103573c4a77a539179a5772da9c", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/f5802103573c4a77a539179a5772da9c.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/f5802103573c4a77a539179a5772da9c"}}, "title": "Increased calcification by erythrophagocytosis in aortic valvular interstitial cells.", "authors": [{"family": "Qin", "given": "Zihan", "initials": "Z"}, {"family": "B\u00e4ck", "given": "Magnus", "initials": "M", "orcid": "0000-0003-0853-5141", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/16eee4e6ca81489389f2c87675a66922.json"}}, {"family": "Franco-Cereceda", "given": "Anders", "initials": "A"}, {"family": "Pawelzik", "given": "Sven-Christian", "initials": "SC"}], "type": "journal article", "published": "2025-04-00", "journal": {"title": "ESC Heart Fail", "issn": "2055-5822", "volume": "12", "issue": "2", "pages": "1469-1473", "issn-l": null}, "abstract": "Calcific aortic valve disease (CAVD) progresses over time to severe aortic stenosis and eventually heart failure. Recent evidence indicates that intraleaflet haemorrhage (ILH) strongly promotes CAVD progression. However, it remains poorly understood how it mechanistically contributes to valvular calcification.\n\nILH was identified as iron deposition by morphological analysis. To elucidate the underlying mechanism, human valvular interstitial cells (VIC) were cultured in the presence of fresh or senescent red blood cells (RBC), simulating ILH in vivo conditions.\n\nILH was common in aortic valves derived from patients with severe aortic stenosis. VIC undergo erythrophagocytosis of senescent RBC, leading to intracellular iron accumulation analogous to observed following exposure to extracellular iron. The presence of senescent RBC significantly intensified VIC calcification, which was significantly mitigated by ferroptosis inhibition.\n\nOur results identify erythrophagocytosis by VIC, leading to iron accumulation and enhanced calcification through ferroptosis. This may be a crucial component of the pathophysiological mechanisms that links ILH to valvular calcification and accelerated aortic stenosis progression.", "doi": "10.1002/ehf2.15132", "pmid": "39462174", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC11911627"}], "notes": [], "created": "2026-09-23T12:25:20.685Z", "modified": "2026-09-23T12:25:20.784Z"}, {"entity": "publication", "iuid": "689bbc19a4fc42f8b8cdd76735d8e48b", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/689bbc19a4fc42f8b8cdd76735d8e48b.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/689bbc19a4fc42f8b8cdd76735d8e48b"}}, "title": "Palmdelphin Regulates Nuclear Resilience to Mechanical Stress in the Endothelium.", "authors": [{"family": "S\u00e1inz-Jaspeado", "given": "Miguel", "initials": "M"}, {"family": "Smith", "given": "Ross O", "initials": "RO", "orcid": "0000-0003-4239-3204", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f597e3f2a2a142c5b0dc7e1559f800b7.json"}}, {"family": "Plunde", "given": "Oscar", "initials": "O"}, {"family": "Pawelzik", "given": "Sven-Christian", "initials": "SC"}, {"family": "Jin", "given": "Yi", "initials": "Y", "orcid": "0000-0001-9704-973X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/69ee4790c8f24da08ba6cf7759d254db.json"}}, {"family": "Nordling", "given": "Sofia", "initials": "S"}, {"family": "Ding", "given": "Yindi", "initials": "Y", "orcid": "0000-0003-4672-7611", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/07381e049bc3491da307b6550f7e0f71.json"}}, {"family": "Aspenstr\u00f6m", "given": "Pontus", "initials": "P"}, {"family": "Hedlund", "given": "Marie", "initials": "M"}, {"family": "Bastianello", "given": "Giulia", "initials": "G"}, {"family": "Ascione", "given": "Flora", "initials": "F"}, {"family": "Li", "given": "Qingsen", "initials": "Q"}, {"family": "Demir", "given": "Cansaran Saygili", "initials": "CS"}, {"family": "Fernando", "given": "Dinesh", "initials": "D", "orcid": "0000-0003-2487-0599", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c881854d6ea84fd4af22950dcdcc8724.json"}}, {"family": "Daniel", "given": "Geoffrey", "initials": "G", "orcid": "0000-0002-8886-1942", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/132ab222d184459a9f69015e577f205d.json"}}, {"family": "Franco-Cereceda", "given": "Anders", "initials": "A"}, {"family": "Kroon", "given": "Jeffrey", "initials": "J", "orcid": "0000-0001-9983-6614", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/2d2942740fcf46e0b559a0e1181c6424.json"}}, {"family": "Foiani", "given": "Marco", "initials": "M"}, {"family": "Petrova", "given": "Tatiana V", "initials": "TV"}, {"family": "Kilimann", "given": "Manfred W", "initials": "MW"}, {"family": "B\u00e4ck", "given": "Magnus", "initials": "M", "orcid": "0000-0003-0853-5141", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/16eee4e6ca81489389f2c87675a66922.json"}}, {"family": "Claesson-Welsh", "given": "Lena", "initials": "L", "orcid": "0000-0003-4275-2000", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6b07fbf00dad4ac8a4a53402888d55ef.json"}}], "type": "journal article", "published": "2021-11-16", "journal": {"title": "Circulation", "issn": "1524-4539", "volume": "144", "issue": "20", "pages": "1629-1645", "issn-l": "0009-7322"}, "abstract": "PALMD (palmdelphin) belongs to the family of paralemmin proteins implicated in cytoskeletal regulation. Single nucleotide polymorphisms in the PALMD locus that result in reduced expression are strong risk factors for development of calcific aortic valve stenosis and predict severity of the disease.\n\nImmunodetection and public database screening showed dominant expression of PALMD in endothelial cells (ECs) in brain and cardiovascular tissues including aortic valves. Mass spectrometry, coimmunoprecipitation, and immunofluorescent staining allowed identification of PALMD partners. The consequence of loss of PALMD expression was assessed in small interferring RNA-treated EC cultures, knockout mice, and human valve samples. RNA sequencing of ECs and transcript arrays on valve samples from an aortic valve study cohort including patients with the single nucleotide polymorphism rs7543130 informed about gene regulatory changes.\n\nECs express the cytosolic PALMD-KKVI splice variant, which associated with RANGAP1 (RAN GTP hydrolyase activating protein 1). RANGAP1 regulates the activity of the GTPase RAN and thereby nucleocytoplasmic shuttling via XPO1 (Exportin1). Reduced PALMD expression resulted in subcellular relocalization of RANGAP1 and XPO1, and nuclear arrest of the XPO1 cargoes p53 and p21. This indicates an important role for PALMD in nucleocytoplasmic transport and consequently in gene regulation because of the effect on localization of transcriptional regulators. Changes in EC responsiveness on loss of PALMD expression included failure to form a perinuclear actin cap when exposed to flow, indicating lack of protection against mechanical stress. Loss of the actin cap correlated with misalignment of the nuclear long axis relative to the cell body, observed in PALMD-deficient ECs, Palmd mouse aorta, and human aortic valve samples derived from patients with calcific aortic valve stenosis. In agreement with these changes in EC behavior, gene ontology analysis showed enrichment of nuclear- and cytoskeleton-related terms in -/-PALMD-silenced ECs.\n\nWe identify RANGAP1 as a PALMD partner in ECs. Disrupting the PALMD/RANGAP1 complex alters the subcellular localization of RANGAP1 and XPO1, and leads to nuclear arrest of the XPO1 cargoes p53 and p21, accompanied by gene regulatory changes and loss of actin-dependent nuclear resilience. Combined, these consequences of reduced PALMD expression provide a mechanistic underpinning for PALMD's contribution to calcific aortic valve stenosis pathology.", "doi": "10.1161/CIRCULATIONAHA.121.054182", "pmid": "34636652", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8589083"}], "notes": [], "created": "2026-09-23T09:52:47.976Z", "modified": "2026-09-23T10:26:47.207Z"}]}