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Specific therapies targeting maladaptive ER stress signaling are lacking. We show that an antisense oligonucleotide (ASO)\u2013based approach reducing CHOP expression ameliorates DKD in mice, providing renal protection on top of ACE inhibition. CHOP inhibition improves both glomerular and tubular damage. ASO-based therapies are a potentially new approach to target maladaptive ER stress signaling and improve DKD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Maladaptive endoplasmic reticulum stress signaling in diabetic kidney disease (DKD) is linked to increased glomerular and tubular expression of the cell-death\u2013promoting transcription factor C\/EBP homologous protein (CHOP). Here, we determined whether locked nucleic acid (LNA)\u2013modified antisense oligonucleotides (ASOs) targeting CHOP ameliorate experimental DKD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We determined the efficacy of CHOP-ASO in the early and late stages of experimental DKD (in 8- or 16-week-old db\/db mice, respectively) alone or with an angiotensin-converting enzyme inhibitor (ACEi), after an\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      dose-escalation study. We used renal functional parameters and morphologic analyses to assess the effect of CHOP-ASO and renal gene-expression profiling to identify differentially regulated genes and pathways. Several human CHOP-ASOs were tested in hyperglycemia-exposed human kidney cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      CHOP-ASOs efficiently reduced renal CHOP expression in diabetic mice and reduced markers of DKD at the early and late stages. Early combined intervention (CHOP-ASO and ACEi) efficiently prevented interstitial damage. At the later timepoint, the combined treatment reduced indices of both glomerular and tubular damage more efficiently than either intervention alone. CHOP-ASO affected a significantly larger number of genes and disease pathways, including reduced sodium-glucose transport protein 2 (Slc5a2) and PROM1 (CD133). Human CHOP-ASOs efficiently reduced glucose-induced CHOP and prevented death of human kidney cells\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The ASO-based approach efficiently reduced renal CHOP expression in a diabetic mouse model, providing an additional benefit to an ACEi, particularly at later timepoints. These studies demonstrate that ASO-based therapies efficiently reduce maladaptive CHOP expression and ameliorate experimental DKD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2021040431","type":"journal-article","created":{"date-parts":[[2021,9,3]],"date-time":"2021-09-03T14:10:33Z","timestamp":1630678233000},"page":"3066-3079","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":27,"title":["CHOP-ASO Ameliorates Glomerular and Tubular Damage on Top of ACE Inhibition in Diabetic Kidney Disease"],"prefix":"10.1681","volume":"32","author":[{"given":"Khurrum","family":"Shahzad","sequence":"first","affiliation":[{"name":"Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, Department of Diagnostics, University Hospital Leipzig, Leipzig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sameen","family":"Fatima","sequence":"additional","affiliation":[{"name":"Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, Department of Diagnostics, University Hospital Leipzig, Leipzig, Germany"},{"name":"Institute of Experimental Internal Medicine, Department of Internal Medicine, Otto-von-Guericke University Magdeburg, Magdeburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Moh\u2019d Mohanad","family":"Al-Dabet","sequence":"additional","affiliation":[{"name":"Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, Department of Diagnostics, University Hospital Leipzig, Leipzig, Germany"},{"name":"Department of Medical Laboratories, American University of Madaba, Amman, Jordan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ihsan","family":"Gadi","sequence":"additional","affiliation":[{"name":"Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, Department of Diagnostics, University Hospital Leipzig, Leipzig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hamzah","family":"Khawaja","sequence":"additional","affiliation":[{"name":"Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, Department of Diagnostics, University Hospital Leipzig, Leipzig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saira","family":"Ambreen","sequence":"additional","affiliation":[{"name":"Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, Department of Diagnostics, University Hospital Leipzig, Leipzig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahmed","family":"Elwakiel","sequence":"additional","affiliation":[{"name":"Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, Department of Diagnostics, University Hospital Leipzig, Leipzig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nora","family":"Kl\u00f6ting","sequence":"additional","affiliation":[{"name":"Helmholtz Institute for Metabolic, Obesity and Vascular Research of the Helmholtz Zentrum M\u00fcnchen at the University of Leipzig, Leipzig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias","family":"Bl\u00fcher","sequence":"additional","affiliation":[{"name":"Helmholtz Institute for Metabolic, Obesity and Vascular Research of the Helmholtz Zentrum M\u00fcnchen at the University of Leipzig, Leipzig, Germany"},{"name":"Medical Department III, Endocrinology, Nephrology, Rheumatology, University Hospital Leipzig, Leipzig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter P.","family":"Nawroth","sequence":"additional","affiliation":[{"name":"Internal Medicine I and Clinical Chemistry, German Diabetes Center, Department of Internal Medicine, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter R.","family":"Mertens","sequence":"additional","affiliation":[{"name":"Clinic of Nephrology and Hypertension, Diabetes and Endocrinology, Department of Internal Medicine, Otto-von-Guericke University, Magdeburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3604-3187","authenticated-orcid":false,"given":"Sven","family":"Michel","sequence":"additional","affiliation":[{"name":"Secarna Pharmaceuticals GmbH & Co. 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