{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T09:35:24Z","timestamp":1785404124243,"version":"3.56.0"},"posted":{"date-parts":[[2026,6,9]]},"group-title":"Molecular Biology","reference-count":83,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T00:00:00Z","timestamp":1780963200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"funder":[{"award":["R01DK135308-01"],"award-info":[{"award-number":["R01DK135308-01"]}],"id":[{"id":"https:\/\/ror.org\/001d55x84","id-type":"ROR","asserted-by":"publisher"}]},{"award":["R01-DK081646"],"award-info":[{"award-number":["R01-DK081646"]}],"id":[{"id":"https:\/\/ror.org\/001d55x84","id-type":"ROR","asserted-by":"publisher"}]},{"award":["R21-AG082416"],"award-info":[{"award-number":["R21-AG082416"]}],"id":[{"id":"https:\/\/ror.org\/001d55x84","id-type":"ROR","asserted-by":"publisher"}]},{"award":["I01-BX002348"],"award-info":[{"award-number":["I01-BX002348"]}],"id":[{"id":"https:\/\/ror.org\/05rsv9s98","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,6,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>Autosomal dominant polycystic kidney disease (ADPKD) is characterized by progressive cyst expansion, fibrosis and inflammation, leading to kidney failure. Myofibroblasts (MFs) often accumulate around cysts and promote fibrosis and cyst growth, but the cellular mechanisms enabling their pro-cystogenic activity remain unclear. Here we examined the role of autophagy within MFs, on their paracrine stimulation of cyst expansion in ADPKD.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Autophagy was assessed in human ADPKD nephrectomy tissue, primary human ADPKD renal myofibroblasts (ADPKD-MFs) and male RC\/RC mouse model of ADPKD using immunostaining, LC3\/p62 analyses, and transmission electron microscopy. Autophagy in MFs was inhibited pharmacologically in ADPKD-MFs, or by conditional Atg5 deletion in PDGFR\u03b2-expressing renal stromal cells in RC\/RC (RC\/RC;Atg5KO) and wild type (WT;Atg5KO) mice.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>\n                    In human and mouse ADPKD kidneys, we detected LC3 puncta and autophagic organelles within \u03b1SMA-expressing MFs. Inhibition of autophagy in ADPKD-MFs blocked their paracrine stimulation of cyst epithelial cell proliferation\n                    <jats:italic>in vitro<\/jats:italic>\n                    . RC\/RC;Atg5KO mice showed significantly reduced cystic growth, fibrosis, MF abundance, and improved kidney function. WT;Atg5KO mice showed no abnormalities in kidney structure or function. Targeted metabolomics performed on ADPKD cyst epithelial-cell conditioned media (ADPKD-ECs CM) revealed moderate increase in lactate levels compared to normal human kidney epithelial-cell conditioned media. Furthermore, lactate treatment stabilized hypoxia-inducible factor-1\u03b1 (HIF1\u03b1) in myofibroblasts, while pharmacological inhibition of HIF1\u03b1 reduced the expression of autophagy-related genes and impaired autophagic flux.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>These findings reveal that autophagy in MFs is a previously unrecognized driver of cyst expansion and fibrosis in ADPKD. Lactate-mediated HIF1\u03b1 stabilization in MFs promotes autophagy that is required for their paracrine stimulation of cyst epithelial growth. Targeting MF-specific autophagy or its upstream regulators may represent a therapeutic strategy to limit cyst growth and fibrosis in ADPKD.<\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.06.05.730503","type":"posted-content","created":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T04:20:14Z","timestamp":1781065214000},"source":"Crossref","is-referenced-by-count":0,"title":["Myofibroblast- specific autophagy drives cyst growth in autosomal dominant polycystic kidney disease"],"prefix":"10.64898","author":[{"given":"Abeda","family":"Jamadar","sequence":"first","affiliation":[{"name":"Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, KS, USA"},{"name":"Department of Medicine, Division of Nephrology, University of Kansas Medical Center, Kansas City, KS, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Viji","family":"Remadevi","sequence":"additional","affiliation":[{"name":"Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, KS, USA"},{"name":"Department of Medicine, Division of Nephrology, University of Kansas Medical Center, Kansas City, KS, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meekha M","family":"Varghese","sequence":"additional","affiliation":[{"name":"Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, KS, USA"},{"name":"Department of Medicine, Division of Nephrology, University of Kansas Medical Center, Kansas City, KS, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haichun","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Pathology, Microbiology & Immunology, Vanderbilt University Medical Center, Nashville, TN, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vedant P.","family":"Thakkar","sequence":"additional","affiliation":[{"name":"Enabling Technologies Group, Sandford Research, Sioux Falls, SD, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Indra","family":"Chandrasekar","sequence":"additional","affiliation":[{"name":"Enabling Technologies Group, Sandford Research, Sioux Falls, SD, USA"},{"name":"Department of Pediatrics, University of South Dakota, Sioux Falls, SD, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wen-Xing","family":"Ding","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, USA"},{"name":"Department of Internal Medicine, Division of Gastroenterology, Hepatology and Mobility, University of Kansas Medical Center, Kansas City, KS, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Volker H.","family":"Haase","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA"},{"name":"Departments of Cancer Biology, and Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA"},{"name":"Research and Medical Services, Department of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, Tennessee, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Darren P.","family":"Wallace","sequence":"additional","affiliation":[{"name":"Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, KS, USA"},{"name":"Department of Medicine, Division of Nephrology, University of Kansas Medical Center, Kansas City, KS, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0739-9344","authenticated-orcid":false,"given":"Reena","family":"Rao","sequence":"additional","affiliation":[{"name":"Jared Grantham Kidney Institute, University of Kansas Medical Center, Kansas City, KS, USA"},{"name":"Department of Medicine, Division of Nephrology, University of Kansas Medical Center, Kansas City, KS, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"key":"2026061200500651000_2026.06.05.730503v1.1","doi-asserted-by":"publisher","DOI":"10.1053\/j.ackd.2009.12.001"},{"key":"2026061200500651000_2026.06.05.730503v1.2","doi-asserted-by":"crossref","unstructured":"Chapman AB , Devuyst O , Eckardt KU , Gansevoort RT , Harris T , Horie S , et al. 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