Detalhe da pesquisa
1.
Combining three independent pathological stressors induces a heart failure with preserved ejection fraction phenotype.
Am J Physiol Heart Circ Physiol
; 324(4): H443-H460, 2023 04 01.
Artigo
em Inglês
| MEDLINE | ID: mdl-36763506
2.
Effects of maternal hypothyroidism on postnatal cardiomyocyte proliferation and cardiac disease responses of the progeny.
Am J Physiol Heart Circ Physiol
; 325(4): H702-H719, 2023 10 01.
Artigo
em Inglês
| MEDLINE | ID: mdl-37539452
3.
Interaction of the Joining Region in Junctophilin-2 With the L-Type Ca2+ Channel Is Pivotal for Cardiac Dyad Assembly and Intracellular Ca2+ Dynamics.
Circ Res
; 128(1): 92-114, 2021 01 08.
Artigo
em Inglês
| MEDLINE | ID: mdl-33092464
4.
Sex-specific responses to slow progressive pressure overload in a large animal model of HFpEF.
Am J Physiol Heart Circ Physiol
; 323(4): H797-H817, 2022 10 01.
Artigo
em Inglês
| MEDLINE | ID: mdl-36053749
5.
Cortical bone stem cells modify cardiac inflammation after myocardial infarction by inducing a novel macrophage phenotype.
Am J Physiol Heart Circ Physiol
; 321(4): H684-H701, 2021 10 01.
Artigo
em Inglês
| MEDLINE | ID: mdl-34415185
6.
Cortical bone-derived stem cell therapy reduces apoptosis after myocardial infarction.
Am J Physiol Heart Circ Physiol
; 317(4): H820-H829, 2019 10 01.
Artigo
em Inglês
| MEDLINE | ID: mdl-31441690
7.
Role of STIM1 (Stromal Interaction Molecule 1) in Hypertrophy-Related Contractile Dysfunction.
Circ Res
; 121(2): 125-136, 2017 Jul 07.
Artigo
em Inglês
| MEDLINE | ID: mdl-28592415
8.
Cortical Bone Stem Cell Therapy Preserves Cardiac Structure and Function After Myocardial Infarction.
Circ Res
; 121(11): 1263-1278, 2017 Nov 10.
Artigo
em Inglês
| MEDLINE | ID: mdl-28912121
9.
Acute Catecholamine Exposure Causes Reversible Myocyte Injury Without Cardiac Regeneration.
Circ Res
; 119(7): 865-79, 2016 Sep 16.
Artigo
em Inglês
| MEDLINE | ID: mdl-27461939
10.
Remodeling of repolarization and arrhythmia susceptibility in a myosin-binding protein C knockout mouse model.
Am J Physiol Heart Circ Physiol
; 313(3): H620-H630, 2017 Sep 01.
Artigo
em Inglês
| MEDLINE | ID: mdl-28646025
11.
Unique Features of Cortical Bone Stem Cells Associated With Repair of the Injured Heart.
Circ Res
; 117(12): 1024-33, 2015 Dec 04.
Artigo
em Inglês
| MEDLINE | ID: mdl-26472818
12.
Transient receptor potential channels contribute to pathological structural and functional remodeling after myocardial infarction.
Circ Res
; 115(6): 567-580, 2014 Aug 29.
Artigo
em Inglês
| MEDLINE | ID: mdl-25047165
13.
Sorafenib cardiotoxicity increases mortality after myocardial infarction.
Circ Res
; 114(11): 1700-1712, 2014 May 23.
Artigo
em Inglês
| MEDLINE | ID: mdl-24718482
14.
Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms.
Circ Res
; 113(5): 539-52, 2013 Aug 16.
Artigo
em Inglês
| MEDLINE | ID: mdl-23801066
15.
A caveolae-targeted L-type Ca²+ channel antagonist inhibits hypertrophic signaling without reducing cardiac contractility.
Circ Res
; 110(5): 669-74, 2012 Mar 02.
Artigo
em Inglês
| MEDLINE | ID: mdl-22302787
16.
Severe hyperhomocysteinemia promotes bone marrow-derived and resident inflammatory monocyte differentiation and atherosclerosis in LDLr/CBS-deficient mice.
Circ Res
; 111(1): 37-49, 2012 Jun 22.
Artigo
em Inglês
| MEDLINE | ID: mdl-22628578
17.
Hyperphosphorylation of the cardiac ryanodine receptor at serine 2808 is not involved in cardiac dysfunction after myocardial infarction.
Circ Res
; 110(6): 831-40, 2012 Mar 16.
Artigo
em Inglês
| MEDLINE | ID: mdl-22302785
18.
Repair of the injured adult heart involves new myocytes potentially derived from resident cardiac stem cells.
Circ Res
; 108(10): 1226-37, 2011 May 13.
Artigo
em Inglês
| MEDLINE | ID: mdl-21454756
19.
miR-182/183-Rasa1 axis induced macrophage polarization and redox regulation promotes repair after ischemic cardiac injury.
Redox Biol
; 67: 102909, 2023 11.
Artigo
em Inglês
| MEDLINE | ID: mdl-37801856
20.
Ca(2+) influx through L-type Ca(2+) channels and transient receptor potential channels activates pathological hypertrophy signaling.
J Mol Cell Cardiol
; 53(5): 657-67, 2012 Nov.
Artigo
em Inglês
| MEDLINE | ID: mdl-22921230