Transplantation of cardiotrophin-1–expressing myoblasts to the left ventricular wall alleviates the transition from compensatory hypertrophy to congestive heart failure in Dahl salt-sensitive hypertensive rats
We investigated whether autologous transplantation of skeletal myoblasts (MB) transferred with cardiotrophin-1 (CT-1) gene could retard the transition to heart failure (HF) in Dahl salt-sensitive (DS) hypertensive rats. Although MB is a therapeutic candidate for chronic HF, little is known about the...
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| Veröffentlicht in: | Journal of the American College of Cardiology 2004-06, Vol.43 (12), p.2337-2347 |
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| creator | Toh, Ryuji Kawashima, Seinosuke Kawai, Miki Sakoda, Tsuyoshi Ueyama, Tomomi Satomi-Kobayashi, Seimi Hirayama, Sonoko Yokoyama, Mitsuhiro |
| description | We investigated whether autologous transplantation of skeletal myoblasts (MB) transferred with cardiotrophin-1 (CT-1) gene could retard the transition to heart failure (HF) in Dahl salt-sensitive (DS) hypertensive rats.
Although MB is a therapeutic candidate for chronic HF, little is known about the efficiency of this strategy when applied in nonischemic HF. Cardiotrophin-1 has potent hypertrophic and survival effects on cardiac myocytes. We hypothesized that transplantation of CT-1–expressing myoblasts could provide cardioprotective effects against ventricular remodeling in DS hypertensive rats.
The DS rats were fed a high salt diet for 6 weeks and developed left ventricular (LV) hypertrophy at 11 weeks. At this stage, animals underwent MB to the myocardium with skeletal myoblasts transferred with CT-1 gene using retrovirus (transplantation of CT-1–expressing myoblasts [MB + CT], n = 31) or myoblasts alone (MB, n = 31). The sham group rats were injected with phosphate-buffered saline (n = 24).
At 17 weeks, MB and MB + CT groups showed a significant alleviation of LV dilation and contractile dysfunction compared with the sham group. The degree of alleviation was significantly greater in the MB + CT group than the MB group (LV end-diastolic dimension: sham 7.06 ± 0.14 mm, MB 6.51 ± 0.16 mm, MB + CT 6.24 ± 0.07 mm; fractional shortening: sham 32.1 ± 1.4%, MB 38.5 ± 1.5%, MB + CT 43.2 ± 0.8%). Histological examination revealed that the myocyte size was 20% larger in the MB + CT group at 17 weeks than in the age-matched sham group. Upregulation of renin-angiotensin and endothelin systems during the transition to HF was attenuated by myoblast transplantation, and this effect was enhanced in the MB + CT group.
Transplantation of skeletal myoblasts combined with CT-1-gene transfer could be a useful therapeutic strategy for HF. |
| doi_str_mv | 10.1016/j.jacc.2004.02.048 |
| format | Article |
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Although MB is a therapeutic candidate for chronic HF, little is known about the efficiency of this strategy when applied in nonischemic HF. Cardiotrophin-1 has potent hypertrophic and survival effects on cardiac myocytes. We hypothesized that transplantation of CT-1–expressing myoblasts could provide cardioprotective effects against ventricular remodeling in DS hypertensive rats.
The DS rats were fed a high salt diet for 6 weeks and developed left ventricular (LV) hypertrophy at 11 weeks. At this stage, animals underwent MB to the myocardium with skeletal myoblasts transferred with CT-1 gene using retrovirus (transplantation of CT-1–expressing myoblasts [MB + CT], n = 31) or myoblasts alone (MB, n = 31). The sham group rats were injected with phosphate-buffered saline (n = 24).
At 17 weeks, MB and MB + CT groups showed a significant alleviation of LV dilation and contractile dysfunction compared with the sham group. The degree of alleviation was significantly greater in the MB + CT group than the MB group (LV end-diastolic dimension: sham 7.06 ± 0.14 mm, MB 6.51 ± 0.16 mm, MB + CT 6.24 ± 0.07 mm; fractional shortening: sham 32.1 ± 1.4%, MB 38.5 ± 1.5%, MB + CT 43.2 ± 0.8%). Histological examination revealed that the myocyte size was 20% larger in the MB + CT group at 17 weeks than in the age-matched sham group. Upregulation of renin-angiotensin and endothelin systems during the transition to HF was attenuated by myoblast transplantation, and this effect was enhanced in the MB + CT group.
Transplantation of skeletal myoblasts combined with CT-1-gene transfer could be a useful therapeutic strategy for HF.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/j.jacc.2004.02.048</identifier><identifier>PMID: 15193703</identifier><identifier>CODEN: JACCDI</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Age ; Animals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Biomarkers - blood ; Blood and lymphatic vessels ; Blood Pressure - drug effects ; Cardiology ; Cardiology. Vascular system ; Cell cycle ; Cell Survival - drug effects ; Cell Transplantation ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Cytokines - genetics ; Cytokines - metabolism ; Cytokines - pharmacology ; Cytomegalovirus ; Deoxyribonucleic acid ; Diastole - drug effects ; Disease Models, Animal ; DNA ; Echocardiography ; Electrocardiography, Ambulatory ; Gene Transfer Techniques ; Heart ; Heart attacks ; Heart failure ; Heart Failure - physiopathology ; Heart Failure - therapy ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Heart rate ; Heart Ventricles - diagnostic imaging ; Heart Ventricles - drug effects ; Heart Ventricles - metabolism ; Hypertension ; Hypertrophy, Left Ventricular - physiopathology ; Hypertrophy, Left Ventricular - therapy ; Male ; Medical sciences ; Models, Cardiovascular ; Myoblasts, Skeletal - transplantation ; Myocardial Contraction - drug effects ; Myocardium - cytology ; Myocardium - metabolism ; Myocardium - pathology ; Neurotransmitter Agents - metabolism ; Ostomy ; Polymerase chain reaction ; Rats ; Rats, Inbred Dahl ; Rodents ; Salt ; Studies ; Up-Regulation - drug effects ; Vasodilation - drug effects ; Ventricular Remodeling - drug effects</subject><ispartof>Journal of the American College of Cardiology, 2004-06, Vol.43 (12), p.2337-2347</ispartof><rights>2004 American College of Cardiology Foundation</rights><rights>2004 INIST-CNRS</rights><rights>Copyright Elsevier Limited Jun 16, 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c512t-8bfcf88bf5d911d9ce5b5d403e73cf1c8506b027f6faf9f339bf4147a30315073</citedby><cites>FETCH-LOGICAL-c512t-8bfcf88bf5d911d9ce5b5d403e73cf1c8506b027f6faf9f339bf4147a30315073</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0735109704005960$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15898134$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15193703$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Toh, Ryuji</creatorcontrib><creatorcontrib>Kawashima, Seinosuke</creatorcontrib><creatorcontrib>Kawai, Miki</creatorcontrib><creatorcontrib>Sakoda, Tsuyoshi</creatorcontrib><creatorcontrib>Ueyama, Tomomi</creatorcontrib><creatorcontrib>Satomi-Kobayashi, Seimi</creatorcontrib><creatorcontrib>Hirayama, Sonoko</creatorcontrib><creatorcontrib>Yokoyama, Mitsuhiro</creatorcontrib><title>Transplantation of cardiotrophin-1–expressing myoblasts to the left ventricular wall alleviates the transition from compensatory hypertrophy to congestive heart failure in Dahl salt-sensitive hypertensive rats</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description>We investigated whether autologous transplantation of skeletal myoblasts (MB) transferred with cardiotrophin-1 (CT-1) gene could retard the transition to heart failure (HF) in Dahl salt-sensitive (DS) hypertensive rats.
Although MB is a therapeutic candidate for chronic HF, little is known about the efficiency of this strategy when applied in nonischemic HF. Cardiotrophin-1 has potent hypertrophic and survival effects on cardiac myocytes. We hypothesized that transplantation of CT-1–expressing myoblasts could provide cardioprotective effects against ventricular remodeling in DS hypertensive rats.
The DS rats were fed a high salt diet for 6 weeks and developed left ventricular (LV) hypertrophy at 11 weeks. At this stage, animals underwent MB to the myocardium with skeletal myoblasts transferred with CT-1 gene using retrovirus (transplantation of CT-1–expressing myoblasts [MB + CT], n = 31) or myoblasts alone (MB, n = 31). The sham group rats were injected with phosphate-buffered saline (n = 24).
At 17 weeks, MB and MB + CT groups showed a significant alleviation of LV dilation and contractile dysfunction compared with the sham group. The degree of alleviation was significantly greater in the MB + CT group than the MB group (LV end-diastolic dimension: sham 7.06 ± 0.14 mm, MB 6.51 ± 0.16 mm, MB + CT 6.24 ± 0.07 mm; fractional shortening: sham 32.1 ± 1.4%, MB 38.5 ± 1.5%, MB + CT 43.2 ± 0.8%). Histological examination revealed that the myocyte size was 20% larger in the MB + CT group at 17 weeks than in the age-matched sham group. Upregulation of renin-angiotensin and endothelin systems during the transition to HF was attenuated by myoblast transplantation, and this effect was enhanced in the MB + CT group.
Transplantation of skeletal myoblasts combined with CT-1-gene transfer could be a useful therapeutic strategy for HF.</description><subject>Age</subject><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - blood</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiology</subject><subject>Cardiology. Vascular system</subject><subject>Cell cycle</subject><subject>Cell Survival - drug effects</subject><subject>Cell Transplantation</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Cytokines - pharmacology</subject><subject>Cytomegalovirus</subject><subject>Deoxyribonucleic acid</subject><subject>Diastole - drug effects</subject><subject>Disease Models, Animal</subject><subject>DNA</subject><subject>Echocardiography</subject><subject>Electrocardiography, Ambulatory</subject><subject>Gene Transfer Techniques</subject><subject>Heart</subject><subject>Heart attacks</subject><subject>Heart failure</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Failure - therapy</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Heart rate</subject><subject>Heart Ventricles - diagnostic imaging</subject><subject>Heart Ventricles - drug effects</subject><subject>Heart Ventricles - metabolism</subject><subject>Hypertension</subject><subject>Hypertrophy, Left Ventricular - physiopathology</subject><subject>Hypertrophy, Left Ventricular - therapy</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Models, Cardiovascular</subject><subject>Myoblasts, Skeletal - transplantation</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardium - cytology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Neurotransmitter Agents - metabolism</subject><subject>Ostomy</subject><subject>Polymerase chain reaction</subject><subject>Rats</subject><subject>Rats, Inbred Dahl</subject><subject>Rodents</subject><subject>Salt</subject><subject>Studies</subject><subject>Up-Regulation - drug effects</subject><subject>Vasodilation - drug effects</subject><subject>Ventricular Remodeling - drug effects</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU2O1DAQhSMEYpqBC7BAlhDs0thx3EkkNqPhVxqJzbC2HKc87ZZjB5fT0DvuwNG4ASfB6W4JxIJF2Srpq_dK9YriKaNrRtnm1W69U1qvK0rrNa3WtG7vFSsmRFty0TX3ixVtuCgZ7ZqL4hHijlK6aVn3sLhggnW8oXxV_LyNyuPklE8q2eBJMESrONiQYpi21pfs1_cf8G2KgGj9HRkPoXcKE5IUSNoCcWAS2YNP0erZqUi-KudILthblQCPUFpc7NHAxDASHcYJPKoU4oFsDxPEo91hEdXB3wEmuweyBRUTMcq6OQKxnrxRW0dQuVQiHAUX6Di-tLmJKuHj4oFRDuHJ-b8sPr97e3v9obz59P7j9dVNqQWrUtn2Rps2v2LoGBs6DaIXQ005NFwbpltBNz2tGrMxynSG8643NasbxSlnIt_2snh50p1i-DLnleVoUYPLx4Qwo2wqypq26TL4_B9wF-bo824yC21y1XWdqepE6RgQIxg5RTuqeJCMyiVwuZNL4HIJXNJK5sDz0LOz9NyPMPwZOSecgRdnQKFWzuQgtMW_uLZrGV_cX584yBfbW4gStQWvYbARdJJDsP_b4zdG5dGZ</recordid><startdate>20040616</startdate><enddate>20040616</enddate><creator>Toh, Ryuji</creator><creator>Kawashima, Seinosuke</creator><creator>Kawai, Miki</creator><creator>Sakoda, Tsuyoshi</creator><creator>Ueyama, Tomomi</creator><creator>Satomi-Kobayashi, Seimi</creator><creator>Hirayama, Sonoko</creator><creator>Yokoyama, Mitsuhiro</creator><general>Elsevier Inc</general><general>Elsevier Science</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20040616</creationdate><title>Transplantation of cardiotrophin-1–expressing myoblasts to the left ventricular wall alleviates the transition from compensatory hypertrophy to congestive heart failure in Dahl salt-sensitive hypertensive rats</title><author>Toh, Ryuji ; Kawashima, Seinosuke ; Kawai, Miki ; Sakoda, Tsuyoshi ; Ueyama, Tomomi ; Satomi-Kobayashi, Seimi ; Hirayama, Sonoko ; Yokoyama, Mitsuhiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c512t-8bfcf88bf5d911d9ce5b5d403e73cf1c8506b027f6faf9f339bf4147a30315073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Age</topic><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - blood</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiology</topic><topic>Cardiology. Vascular system</topic><topic>Cell cycle</topic><topic>Cell Survival - drug effects</topic><topic>Cell Transplantation</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Cytokines - pharmacology</topic><topic>Cytomegalovirus</topic><topic>Deoxyribonucleic acid</topic><topic>Diastole - drug effects</topic><topic>Disease Models, Animal</topic><topic>DNA</topic><topic>Echocardiography</topic><topic>Electrocardiography, Ambulatory</topic><topic>Gene Transfer Techniques</topic><topic>Heart</topic><topic>Heart attacks</topic><topic>Heart failure</topic><topic>Heart Failure - physiopathology</topic><topic>Heart Failure - therapy</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Heart rate</topic><topic>Heart Ventricles - diagnostic imaging</topic><topic>Heart Ventricles - drug effects</topic><topic>Heart Ventricles - metabolism</topic><topic>Hypertension</topic><topic>Hypertrophy, Left Ventricular - physiopathology</topic><topic>Hypertrophy, Left Ventricular - therapy</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Models, Cardiovascular</topic><topic>Myoblasts, Skeletal - transplantation</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardium - cytology</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Neurotransmitter Agents - metabolism</topic><topic>Ostomy</topic><topic>Polymerase chain reaction</topic><topic>Rats</topic><topic>Rats, Inbred Dahl</topic><topic>Rodents</topic><topic>Salt</topic><topic>Studies</topic><topic>Up-Regulation - drug effects</topic><topic>Vasodilation - drug effects</topic><topic>Ventricular Remodeling - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Toh, Ryuji</creatorcontrib><creatorcontrib>Kawashima, Seinosuke</creatorcontrib><creatorcontrib>Kawai, Miki</creatorcontrib><creatorcontrib>Sakoda, Tsuyoshi</creatorcontrib><creatorcontrib>Ueyama, Tomomi</creatorcontrib><creatorcontrib>Satomi-Kobayashi, Seimi</creatorcontrib><creatorcontrib>Hirayama, Sonoko</creatorcontrib><creatorcontrib>Yokoyama, Mitsuhiro</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of the American College of Cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Toh, Ryuji</au><au>Kawashima, Seinosuke</au><au>Kawai, Miki</au><au>Sakoda, Tsuyoshi</au><au>Ueyama, Tomomi</au><au>Satomi-Kobayashi, Seimi</au><au>Hirayama, Sonoko</au><au>Yokoyama, Mitsuhiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transplantation of cardiotrophin-1–expressing myoblasts to the left ventricular wall alleviates the transition from compensatory hypertrophy to congestive heart failure in Dahl salt-sensitive hypertensive rats</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>2004-06-16</date><risdate>2004</risdate><volume>43</volume><issue>12</issue><spage>2337</spage><epage>2347</epage><pages>2337-2347</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><coden>JACCDI</coden><abstract>We investigated whether autologous transplantation of skeletal myoblasts (MB) transferred with cardiotrophin-1 (CT-1) gene could retard the transition to heart failure (HF) in Dahl salt-sensitive (DS) hypertensive rats.
Although MB is a therapeutic candidate for chronic HF, little is known about the efficiency of this strategy when applied in nonischemic HF. Cardiotrophin-1 has potent hypertrophic and survival effects on cardiac myocytes. We hypothesized that transplantation of CT-1–expressing myoblasts could provide cardioprotective effects against ventricular remodeling in DS hypertensive rats.
The DS rats were fed a high salt diet for 6 weeks and developed left ventricular (LV) hypertrophy at 11 weeks. At this stage, animals underwent MB to the myocardium with skeletal myoblasts transferred with CT-1 gene using retrovirus (transplantation of CT-1–expressing myoblasts [MB + CT], n = 31) or myoblasts alone (MB, n = 31). The sham group rats were injected with phosphate-buffered saline (n = 24).
At 17 weeks, MB and MB + CT groups showed a significant alleviation of LV dilation and contractile dysfunction compared with the sham group. The degree of alleviation was significantly greater in the MB + CT group than the MB group (LV end-diastolic dimension: sham 7.06 ± 0.14 mm, MB 6.51 ± 0.16 mm, MB + CT 6.24 ± 0.07 mm; fractional shortening: sham 32.1 ± 1.4%, MB 38.5 ± 1.5%, MB + CT 43.2 ± 0.8%). Histological examination revealed that the myocyte size was 20% larger in the MB + CT group at 17 weeks than in the age-matched sham group. Upregulation of renin-angiotensin and endothelin systems during the transition to HF was attenuated by myoblast transplantation, and this effect was enhanced in the MB + CT group.
Transplantation of skeletal myoblasts combined with CT-1-gene transfer could be a useful therapeutic strategy for HF.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>15193703</pmid><doi>10.1016/j.jacc.2004.02.048</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Age Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Biomarkers - blood Blood and lymphatic vessels Blood Pressure - drug effects Cardiology Cardiology. Vascular system Cell cycle Cell Survival - drug effects Cell Transplantation Clinical manifestations. Epidemiology. Investigative techniques. Etiology Cytokines - genetics Cytokines - metabolism Cytokines - pharmacology Cytomegalovirus Deoxyribonucleic acid Diastole - drug effects Disease Models, Animal DNA Echocardiography Electrocardiography, Ambulatory Gene Transfer Techniques Heart Heart attacks Heart failure Heart Failure - physiopathology Heart Failure - therapy Heart failure, cardiogenic pulmonary edema, cardiac enlargement Heart rate Heart Ventricles - diagnostic imaging Heart Ventricles - drug effects Heart Ventricles - metabolism Hypertension Hypertrophy, Left Ventricular - physiopathology Hypertrophy, Left Ventricular - therapy Male Medical sciences Models, Cardiovascular Myoblasts, Skeletal - transplantation Myocardial Contraction - drug effects Myocardium - cytology Myocardium - metabolism Myocardium - pathology Neurotransmitter Agents - metabolism Ostomy Polymerase chain reaction Rats Rats, Inbred Dahl Rodents Salt Studies Up-Regulation - drug effects Vasodilation - drug effects Ventricular Remodeling - drug effects |
| title | Transplantation of cardiotrophin-1–expressing myoblasts to the left ventricular wall alleviates the transition from compensatory hypertrophy to congestive heart failure in Dahl salt-sensitive hypertensive rats |
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