{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T23:17:12Z","timestamp":1788909432911,"version":"build-2803163510"},"reference-count":69,"publisher":"American Society for Clinical Investigation","issue":"9","license":[{"start":{"date-parts":[[2022,5,9]],"date-time":"2022-05-09T00:00:00Z","timestamp":1652054400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"FWF, ERC, Medical University of Graz","award":["DK-MCD (W1226) LipoCheX (340896) LipoLung (P30968)"],"award-info":[{"award-number":["DK-MCD (W1226) LipoCheX (340896) LipoLung (P30968)"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,5,9]]},"abstract":"<jats:p>\n                    The lung airways are constantly exposed to inhaled toxic substances, resulting in cellular damage that is repaired by local expansion of resident bronchiolar epithelial club cells. Disturbed bronchiolar epithelial damage repair lies at the core of many prevalent lung diseases, including chronic obstructive pulmonary disease, asthma, pulmonary fibrosis, and lung cancer. However, it is still not known how bronchiolar club cell energy metabolism contributes to this process. Here, we show that adipose triglyceride lipase (ATGL), the rate-limiting enzyme for intracellular lipolysis, is critical for normal club cell function in mice. Deletion of the gene encoding ATGL,\n                    <jats:italic>Pnpla2<\/jats:italic>\n                    (also known as\n                    <jats:italic>Atgl<\/jats:italic>\n                    ), induced substantial triglyceride accumulation, decreased mitochondrial numbers, and decreased mitochondrial respiration in club cells. This defect manifested as bronchiolar epithelial thickening and increased airway resistance under baseline conditions. After naphthalene\u2011induced epithelial denudation, a regenerative defect was apparent. Mechanistically, dysfunctional PPAR\u03b1 lipid-signaling underlies this phenotype because (a) ATGL was needed for PPAR\u03b1 lipid-signaling in regenerating bronchioles and (b) administration of the specific PPAR\u03b1 agonist WY14643 restored normal bronchiolar club cell ultrastructure and regenerative potential. Our data emphasize the importance of the cellular energy metabolism for lung epithelial regeneration and highlight the significance of ATGL-mediated lipid catabolism for lung health.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.149438","type":"journal-article","created":{"date-parts":[[2022,3,29]],"date-time":"2022-03-29T12:00:52Z","timestamp":1648555252000},"source":"Crossref","is-referenced-by-count":13,"title":["Adipose triglyceride lipase\u2013mediated lipid catabolism is essential for bronchiolar regeneration"],"prefix":"10.1172","volume":"7","author":[{"given":"Manu Manjunath","family":"Kanti","sequence":"first","affiliation":[{"name":"Diagnostic and Research Institute of Pathology, Medical University of Graz, Graz, Austria."},{"name":"BioTechMed-Graz, Graz, Austria."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Isabelle","family":"Striessnig-Bina","sequence":"additional","affiliation":[{"name":"Diagnostic and Research Institute of Pathology, 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