{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T12:36:20Z","timestamp":1789821380638,"version":"4.0.1"},"reference-count":72,"publisher":"Portland Press Ltd.","issue":"2","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,7,1]]},"abstract":"<jats:p>The lungs are the primary organs affected in LHD (left heart disease). Increased left atrial pressure leads to pulmonary alveolar\u2013capillary stress failure, resulting in cycles of alveolar wall injury and repair. The reparative process causes the proliferation of MYFs (myofibroblasts) with fibrosis and extracellular matrix deposition, resulting in thickening of the alveolar wall. Although the resultant reduction in vascular permeability is initially protective against pulmonary oedema, the process becomes maladaptive causing a restrictive lung syndrome with impaired gas exchange. This pathological process may also contribute to PH (pulmonary hypertension) due to LHD. Few clinical trials have specifically evaluated lung structural remodelling and the effect of related therapies in LHD. Currently approved treatment for chronic HF (heart failure) may have direct beneficial effects on lung structural remodelling. In the future, novel therapies specifically targeting the remodelling processes may potentially be utilized. In the present review, we summarize data supporting the clinical importance and pathophysiological mechanisms of lung structural remodelling in LHD and propose that this pathophysiological process should be explored further in pre-clinical studies and future therapeutic trials.<\/jats:p>","DOI":"10.1042\/cs20130296","type":"journal-article","created":{"date-parts":[[2014,3,17]],"date-time":"2014-03-17T12:43:12Z","timestamp":1395060192000},"page":"65-76","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Lung capillary injury and repair in left heart disease: a new target for therapy?"],"prefix":"10.1042","volume":"127","author":[{"given":"Sayena","family":"Azarbar","sequence":"first","affiliation":[{"name":"Department of Medicine, Montreal Heart Institute, Universit\u00e9 de Montr\u00e9al, 5000 Belanger Street, Montreal, Quebec, Canada, H1T 1C8"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jocelyn","family":"Dupuis","sequence":"additional","affiliation":[{"name":"Department of Medicine, Montreal Heart Institute, Universit\u00e9 de Montr\u00e9al, 5000 Belanger Street, Montreal, Quebec, Canada, H1T 1C8"},{"name":"Research Center, Montreal Heart Institute, Universit\u00e9 de Montr\u00e9al, 5000 Belanger Street, Montreal, Quebec, Canada, H1T 1C8"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2014,3,17]]},"reference":[{"key":"2021113010331091700_B1","doi-asserted-by":"crossref","first-page":"622","DOI":"10.1161\/01.CIR.92.3.622","article-title":"Vulnerability of pulmonary capillaries in heart disease","volume":"92","author":"West","year":"1995","journal-title":"Circulation"},{"key":"2021113010331091700_B2","doi-asserted-by":"crossref","first-page":"669","DOI":"10.1378\/chest.125.2.669","article-title":"The pulmonary manifestations of left heart failure","volume":"125","author":"Gehlbach","year":"2004","journal-title":"Chest"},{"key":"2021113010331091700_B3","doi-asserted-by":"crossref","first-page":"233","DOI":"10.1016\/j.ccm.2006.12.001","article-title":"Pulmonary hypertension associated with left-sided heart disease","volume":"28","author":"Oudiz","year":"2007","journal-title":"Clin. 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