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However, a comprehensive molecular basis for altered matrix is not well understood. Ultrastructural and proteomic studies in mouse models of genetic kidney disease and human tissue define a molecular basis for altered matrix, which has common features across aging and disease progression. Broadly, basement membrane components are reduced, interstitial matrix proteins are increased, and this is coupled with altered cell adhesion and metabolic processes. Furthermore, a signature of altered matrix proteins appears before ultrastructural defects and could have utility as biomarkers of kidney health. Mechanistically, this altered kidney matrix may initiate abnormal kidney cell\u2013matrix and immune cell\u2013matrix interactions, which therapy could target.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Accumulation of extracellular matrix in organs and tissues is a feature of both aging and disease. In the kidney, glomerulosclerosis and tubulointerstitial fibrosis accompany the decline in function, which current therapies cannot address, leading to organ failure. Although histologic and ultrastructural patterns of excess matrix form the basis of human disease classifications, a comprehensive molecular resolution of abnormal matrix is lacking.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Using mass spectrometry\u2013based proteomics, we resolved matrix composition over age in mouse models of kidney disease. We compared the changes in mice with a global characterization of human kidneymatrix during aging and to existing kidney disease datasets to identify common molecular features.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Ultrastructural changes in basement membranes are associated with altered cell adhesion and metabolic processes and with distinct matrix proteomes during aging and kidney disease progression in mice. Within the altered matrix, basement membrane components (laminins, type IV collagen, type XVIII collagen) were reduced and interstitial matrix proteins (collagens I, III, VI, and XV; fibrinogens; and nephronectin) were increased, a pattern also seen in human kidney aging. Indeed, this signature of matrix proteins was consistently modulated across all age and disease comparisons, and the increase in interstitial matrix was also observed in human kidney disease datasets.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This study provides deep molecular resolution of matrix accumulation in kidney aging and disease, and identifies a common signature of proteins that provides insight into mechanisms of response to kidney injury and repair.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2020101442","type":"journal-article","created":{"date-parts":[[2021,5,28]],"date-time":"2021-05-28T16:00:22Z","timestamp":1622217622000},"page":"1713-1732","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":77,"title":["Identification of an Altered Matrix Signature in Kidney Aging and Disease"],"prefix":"10.1681","volume":"32","author":[{"given":"Michael J.","family":"Randles","sequence":"first","affiliation":[{"name":"Wellcome Centre for Cell-Matrix Research, Division of Cell-Matrix Biology and Regenerative Medicine, School of Biological Sciences, Faculty of Biology Medicine and Health, The University of Manchester, Manchester Academic Health Science Centre, Manchester, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Franziska","family":"Lausecker","sequence":"additional","affiliation":[{"name":"Wellcome Centre for Cell-Matrix Research, Division of Cell-Matrix Biology and Regenerative Medicine, School of Biological Sciences, Faculty of Biology Medicine and Health, The University of Manchester, Manchester Academic Health Science Centre, Manchester, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qingyang","family":"Kong","sequence":"additional","affiliation":[{"name":"Department of Renal Medicine, University College London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hani","family":"Suleiman","sequence":"additional","affiliation":[{"name":"Renal Division, Washington University School of Medicine, Saint Louis, Missouri"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0881-2209","authenticated-orcid":false,"given":"Graeme","family":"Reid","sequence":"additional","affiliation":[{"name":"Department of Histopathology, Manchester Royal Infirmary, Manchester University Hospitals National Health Service Foundation Trust, Manchester Academic Health Science Centre, Manchester, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Kolatsi-Joannou","sequence":"additional","affiliation":[{"name":"Developmental Biology and Cancer Programme, Great Ormond Institute of Child Health, University College London, London, United 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