{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T06:48:12Z","timestamp":1774594092263,"version":"3.50.1"},"reference-count":60,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T00:00:00Z","timestamp":1774569600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82570887, 82400889, 82070769, 81770751, 82270790, 81470981"],"award-info":[{"award-number":["82570887, 82400889, 82070769, 81770751, 82270790, 81470981"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Advanced renal failure remains a major global health burden. Mitochondrial dysfunction is frequently observed during progressive kidney injury and chronic allograft dysfunction (CAD), but observational data cannot distinguish causal involvement from secondary consequences. We applied a multi-omic genetic prioritization framework to evaluate whether inherited variation affecting mitochondrial gene regulation is associated with a proxy phenotype for advanced renal failure and fibrotic allograft remodeling.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We integrated cis-mQTL (DNA methylation), cis-eQTL (gene expression), and cis-pQTL (plasma protein) data for MitoCarta3.0 genes with a UK Biobank GWAS of kidney transplant recipient status (369 cases, 397,602 controls) as a proxy endpoint for advanced renal failure. Summary-data-based Mendelian randomization (SMR; Wald ratio) was performed using a single lead cis-QTL instrument per gene per layer, with HEIDI heterogeneity testing and Bayesian colocalization to assess whether molecular QTL and outcome signals were consistent with a shared causal variant (PPH4 \u2265 0.70). Because no association survived false discovery rate (FDR) correction across the mitochondrial gene set, we used a tiered, exploratory prioritization scheme based on nominal MR evidence and colocalization. Instrument strength metrics (F-statistics and R\u00b2) are reported.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      At a nominal threshold (\n                      <jats:italic>p<\/jats:italic>\n                      \u00a0&amp;lt;\u00a00.05; none surviving FDR &amp;lt; 0.05), we observed suggestive SMR associations in the methylation and expression layers, with generally weaker signals in the protein layer. Integrating MR evidence with colocalization support prioritized eight mitochondrial candidate genes (\n                      <jats:italic>C20orf72<\/jats:italic>\n                      \/\n                      <jats:italic>MGME1<\/jats:italic>\n                      ,\n                      <jats:italic>NDUFA13<\/jats:italic>\n                      ,\n                      <jats:italic>MRPS18C<\/jats:italic>\n                      ,\n                      <jats:italic>MTIF3<\/jats:italic>\n                      ,\n                      <jats:italic>ECHDC1<\/jats:italic>\n                      ,\n                      <jats:italic>MTHFD1L<\/jats:italic>\n                      ,\n                      <jats:italic>QDPR<\/jats:italic>\n                      , and\n                      <jats:italic>TST<\/jats:italic>\n                      ). Translational evaluation showed dysregulation of several prioritized candidates in human CAD allograft tissues and in a murine allogeneic kidney transplantation model of chronic allograft fibrosis. In TGF-\u03b2\u2013stimulated HK-2 cells, mitochondrial dysfunction accompanied profibrotic responses, and functional perturbation supported\n                      <jats:italic>NDUFA13<\/jats:italic>\n                      as a plausible node linking mitochondrial bioenergetics to fibrotic remodeling.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Given the limited number of outcome cases, the proxy nature of transplant recipient status, and no FDR-significant associations, the genetic results should be interpreted as exploratory and hypothesis-generating rather than causal proof. Nonetheless, multi-omic genetic prioritization with kidney-relevant experimental data highlights mitochondrial pathways as plausible contributors to advanced renal failure and fibrotic allograft remodeling, motivating replication in larger outcome GWAS and kidney-relevant QTL resources.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1783844","type":"journal-article","created":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T05:19:28Z","timestamp":1774588768000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Genetically prioritized mitochondrial regulators of advanced renal failure: multi-omic Mendelian randomization and biological plausibility assessment in allograft fibrosis"],"prefix":"10.3389","volume":"17","author":[{"given":"Qinghuan","family":"Shen","sequence":"first","affiliation":[{"name":"The First Affiliated Hospital with Nanjing Medical University, Department of Urology, 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