학술논문
Mitochondrial Ca 2+ Uniporter-Dependent Energetic Dysfunction Drives Hypertrophy in Heart Failure.
Document Type
Academic Journal
Author
Alves-Figueiredo H; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Vascular, Monterrey, NL, México.; Tecnologico de Monterrey, Institute for Obesity Research, Monterrey, NL, México.; Tecnologico de Monterrey, Hospital Zambrano Hellion, TecSalud, San Pedro Garza García, NL, México.; Silva-Platas C; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Vascular, Monterrey, NL, México.; Estrada M; Programa de Fisiología y Biofísica, Facultad de Medicina, Instituto de Ciencias Biomédicas (ICBM), Universidad de Chile, Santiago, Chile.; Oropeza-Almazán Y; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Vascular, Monterrey, NL, México.; Ramos-González M; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Vascular, Monterrey, NL, México.; Bernal-Ramírez J; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Vascular, Monterrey, NL, México.; Tecnologico de Monterrey, Institute for Obesity Research, Monterrey, NL, México.; Vázquez-Garza E; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Vascular, Monterrey, NL, México.; Tecnologico de Monterrey, Institute for Obesity Research, Monterrey, NL, México.; Tellez A; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Vascular, Monterrey, NL, México.; Alizée Pathology, Thurmont, Maryland, USA.; Salazar-Ramírez F; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Vascular, Monterrey, NL, México.; Méndez-Fernández A; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Vascular, Monterrey, NL, México.; Galaz JL; Programa de Fisiología y Biofísica, Facultad de Medicina, Instituto de Ciencias Biomédicas (ICBM), Universidad de Chile, Santiago, Chile.; Lobos P; Programa de Fisiología y Biofísica, Facultad de Medicina, Instituto de Ciencias Biomédicas (ICBM), Universidad de Chile, Santiago, Chile.; Youker K; Weill Cornell Medical College, Methodist DeBakey Heart & Vascular Center, The Methodist Hospital, Houston, Texas, USA.; Lozano O; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Vascular, Monterrey, NL, México.; Tecnologico de Monterrey, Institute for Obesity Research, Monterrey, NL, México.; Tecnologico de Monterrey, Hospital Zambrano Hellion, TecSalud, San Pedro Garza García, NL, México.; Torre-Amione G; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Vascular, Monterrey, NL, México.; Tecnologico de Monterrey, Hospital Zambrano Hellion, TecSalud, San Pedro Garza García, NL, México.; Weill Cornell Medical College, Methodist DeBakey Heart & Vascular Center, The Methodist Hospital, Houston, Texas, USA.; García-Rivas G; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Cátedra de Cardiología y Medicina Vascular, Monterrey, NL, México.; Tecnologico de Monterrey, Institute for Obesity Research, Monterrey, NL, México.; Tecnologico de Monterrey, Hospital Zambrano Hellion, TecSalud, San Pedro Garza García, NL, México.
Source
Publisher: Elsevier on behalf of the American College of Cardiology Foundation Country of Publication: United States NLM ID: 101677259 Publication Model: eCollection Cited Medium: Internet ISSN: 2452-302X (Electronic) Linking ISSN: 2452302X NLM ISO Abbreviation: JACC Basic Transl Sci Subsets: PubMed not MEDLINE
Subject
Language
English
Abstract
The role of the mitochondrial calcium uniporter (MCU) in energy dysfunction and hypertrophy in heart failure (HF) remains unknown. In angiotensin II (ANGII)-induced hypertrophic cardiac cells we have shown that hypertrophic cells overexpress MCU and present bioenergetic dysfunction. However, by silencing MCU, cell hypertrophy and mitochondrial dysfunction are prevented by blocking mitochondrial calcium overload, increase mitochondrial reactive oxygen species, and activation of nuclear factor kappa B-dependent hypertrophic and proinflammatory signaling. Moreover, we identified a calcium/calmodulin-independent protein kinase II/cyclic adenosine monophosphate response element-binding protein signaling modulating MCU upregulation by ANGII. Additionally, we found upregulation of MCU in ANGII-induced left ventricular HF in mice, and in the LV of HF patients, which was correlated with pathological remodeling. Following left ventricular assist device implantation, MCU expression decreased, suggesting tissue plasticity to modulate MCU expression.
Competing Interests: This work was partially supported by the CONACYT Grants 256577, 258197, Fronteras de la Ciencia Grant (0682). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
(© 2024 The Authors.)
Competing Interests: This work was partially supported by the CONACYT Grants 256577, 258197, Fronteras de la Ciencia Grant (0682). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
(© 2024 The Authors.)