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Grant support

This research was funded by Instituto de Salud Carlos III (ISCIII)-Fondo de Investigacion Sanitaria (FIS)-Fondo Europeo de Desarrollo Regional FEDER grants PI19/00588 and PI19/00815 and by Sociedad Espanola de Nefrologia grant 9749/004. Salary support was from ISCIII Miguel Servet (to N. MendezBarbero), ISCIII predoctoral contract of Training in Investigation in Health PFIS (to A.M. Lopez-Diaz), Ministerio de Ciencia, Innovaci~on y Universidades (to J. Guerrero-Mauvecin), Red de Investigacion Renal (REDINREN) grant RD016/0009 (to M. Fontecha-Barriuso), and Ramon y Cajal program (to M.D. Sanchez-Ni~no and A.B. Sanz). We acknowledge Comunidad de Madrid en Biomedicina grant B2017/BMD-3686 CIFRA2-CM; FRIAT; IIS-Fundacion Jimenez Diaz Biobank grant PT17/0015/0006; and Instituto de Salud Carlos III FIS/FEDER grants PI17/00257, PI17/00119, PI20/00140, PI18/01366, PI20/00639, PI21/01126, DTS18/00032, European Research Area-PerMed-JTC2018 KIDNEY ATTACK AC18/00064 and Personalized treatment in IgA Nephropathy (PERSTIGAN) AC18/00071 and ISCIII-Redes tematicas de investigacion cooperativa en salud (RETICS) REDinREN RD016/0009.

Analysis of institutional authors

Sanchez-Nino, Maria DAuthorCannata-Ortiz, PabloAuthorRuiz-Ortega, MartaAuthorOrtiz, AlbertoCorresponding Author

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October 3, 2024
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Bone Marrow-Derived RIPK3 Mediates Kidney Inflammation in Acute Kidney Injury

Publicated to:JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY. 33 (2): 357-373 - 2022-01-19 33(2), DOI: 10.1681/ASN.2021030383

Authors: Martin-Sanchez, Diego; Guerrero-Mauvecin, Juan; Fontecha-Barriuso, Miguel; Mendez-Barbero, Nerea; Laura Saiz, Maria; Lopez-Diaz, Ana M; Sanchez-Nino, Maria D; Carrasco, Susana; Cannata-Ortiz, Pablo; Ruiz-Ortega, Marta; Ortiz, Alberto; Sanz, Ana B

Affiliations

Ctr Invest Biomed Red Enfermedades Cardiovasc, Madrid, Spain - Author
Inst Invest Sanitaria Principado Asturias, Translat Immunol Lab, Oviedo, Spain - Author
Inst Reina Sofia Invest Nefrol, Madrid, Spain - Author
Red Invest Renal, Madrid, Spain - Author
Univ Autonoma Madrid, Dept Med, Madrid, Spain - Author
Univ Autonoma Madrid, Dept Pharmacol, Madrid, Spain - Author
Univ Autonoma Madrid, Inst Invest Sanitaria Fdn Jimenez Diaz, Dept Pathol, Madrid, Spain - Author
Univ Autonoma Madrid, Inst Invest Sanitaria Fdn Jimenez Diaz, Lab Nefrol Expt, Madrid, Spain - Author
Univ Autonoma Madrid, Inst Invest Sanitaria Fdn Jimenez Diaz, Lab Patol Vasc, Madrid, Spain - Author
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Abstract

Background Receptor-interacting protein kinase 3 (RIPK3), a component of necroptosis pathways, may have an independent role in inflammation. It has been unclear which RIPK3-expressing cells are responsible for the anti-inflammatory effect of overall Ripk3 deficiency and whether Ripk3 deficiency protects against kidney inflammation occurring in the absence of tubular cell death. Methods We used chimeric mice with bone marrow from wild-type and Ripk3-knockout mice to explore RIPK39s contribution to kidney inflammation in the presence of folic acid-induced acute kidney injury AKI (FA-AKI) or absence of AKI and kidney cell death (as seen in systemic administration of the cytokine TNFlike weak inducer of apoptosis [TWEAK]). Results Tubular and interstitial cell RIPK3 expressions were increased in murine AKI. Ripk3 deficiency decreased NF- kB activation and kidney inflammation in FA-AKI but did not prevent kidney failure. In the chimeric mice, RIPK3-expressing bone marrow-derived cells were required for early inflammation in FA-AKI. The NLRP3 inflammasome was not involved in RIPK39s proinflammatory effect. Systemic TWEAK administration induced kidney inflammation in wild-type but not Ripk3-deficient mice. In cell cultures, TWEAK increased RIPK3 expression in bone marrow-derived macrophages and tubular cells. RIPK3 mediated TWEAK-induced NF- kB activation and inflammatory responses in bone marrow-derived macrophages and dendritic cells and in Jurkat T cells; however, in tubular cells, RIPK3 mediated only TWEAKinduced Il-6 expression. Furthermore, conditioned media from TWEAK-exposed wild-type macrophages, but not from Ripk3-deficient macrophages, promoted proinflammatory responses in cultured tubular cells. Conclusions RIPK3 mediates kidney inflammation independently from tubular cell death. Specific targeting of bone marrow-derived RIPK3 may limit kidney inflammation without the potential adverse effects of systemic RIPK3 targeting.

Keywords

AcidCell-deathDown-regulationNecroptosiNecrosisTweak

Quality index

Bibliometric impact. Analysis of the contribution and dissemination channel

The work has been published in the journal JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY due to its progression and the good impact it has achieved in recent years, according to the agency WoS (JCR), it has become a reference in its field. In the year of publication of the work, 2022, it was in position 5/88, thus managing to position itself as a Q1 (Primer Cuartil), in the category Urology & Nephrology. Notably, the journal is positioned above the 90th percentile.

From a relative perspective, and based on the normalized impact indicator calculated from World Citations provided by WoS (ESI, Clarivate), it yields a value for the citation normalization relative to the expected citation rate of: 7.36. This indicates that, compared to works in the same discipline and in the same year of publication, it ranks as a work cited above average. (source consulted: ESI Nov 14, 2024)

This information is reinforced by other indicators of the same type, which, although dynamic over time and dependent on the set of average global citations at the time of their calculation, consistently position the work at some point among the top 50% most cited in its field:

  • Weighted Average of Normalized Impact by the Scopus agency: 5.23 (source consulted: FECYT Feb 2024)
  • Field Citation Ratio (FCR) from Dimensions: 13.67 (source consulted: Dimensions Jul 2025)

Specifically, and according to different indexing agencies, this work has accumulated citations as of 2025-07-08, the following number of citations:

  • WoS: 22
  • Scopus: 23

Impact and social visibility

From the perspective of influence or social adoption, and based on metrics associated with mentions and interactions provided by agencies specializing in calculating the so-called "Alternative or Social Metrics," we can highlight as of 2025-07-08:

  • The use, from an academic perspective evidenced by the Altmetric agency indicator referring to aggregations made by the personal bibliographic manager Mendeley, gives us a total of: 20.
  • The use of this contribution in bookmarks, code forks, additions to favorite lists for recurrent reading, as well as general views, indicates that someone is using the publication as a basis for their current work. This may be a notable indicator of future more formal and academic citations. This claim is supported by the result of the "Capture" indicator, which yields a total of: 22 (PlumX).

With a more dissemination-oriented intent and targeting more general audiences, we can observe other more global scores such as:

  • The Total Score from Altmetric: 2.
  • The number of mentions on the social network X (formerly Twitter): 4 (Altmetric).

It is essential to present evidence supporting full alignment with institutional principles and guidelines on Open Science and the Conservation and Dissemination of Intellectual Heritage. A clear example of this is:

  • The work has been submitted to a journal whose editorial policy allows open Open Access publication.

Leadership analysis of institutional authors

There is a significant leadership presence as some of the institution’s authors appear as the first or last signer, detailed as follows: First Author (Martin-Sanchez, Diego) and Last Author (Sanz, Ana B).

the authors responsible for correspondence tasks have been ORTIZ ARDUAN, ALBERTO and Sanz, Ana B.