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Article ; Online: Activation of Phosphodiesterase 3A: New Hope for Cardioprotection.

Chiong, Mario / Houslay, Miles D / Lavandero, Sergio

2022 Volume 146, Issue 23, Page(s) 1779–1782

MeSH term(s)	Humans ; Cyclic Nucleotide Phosphodiesterases, Type 3 ; A Kinase Anchor Proteins/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism
Chemical Substances	Cyclic Nucleotide Phosphodiesterases, Type 3 (EC 3.1.4.17) ; A Kinase Anchor Proteins ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
Language	English
Publishing date	2022-12-05
Publishing country	United States
Document type	Editorial ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.122.062215
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Article ; Online: A new oxime synthesized from

Palacios, Javier / Asunción-Alvarez, Daniel / Aravena, Diego / Chiong, Mario / Catalán, Marcelo A / Parra, Claudio / Cifuentes, Fredi / Paredes, Adrián

RSC advances

2024 Volume 14, Issue 14, Page(s) 9933–9942

Abstract: ... Senecio ... ...

Abstract	Senecio nutans
Language	English
Publishing date	2024-03-25
Publishing country	England
Document type	Journal Article
ISSN	2046-2069
ISSN (online)	2046-2069
DOI	10.1039/d4ra01058b
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Article ; Online: The role of autophagy in cardiovascular pathology.

Gatica, Damián / Chiong, Mario / Lavandero, Sergio / Klionsky, Daniel J

Cardiovascular research

2021 Volume 118, Issue 4, Page(s) 934–950

Abstract: Macroautophagy/autophagy is a conserved catabolic recycling pathway in which cytoplasmic components are sequestered, degraded, and recycled to survive various stress conditions. Autophagy dysregulation has been observed and linked with the development ... ...

Abstract	Macroautophagy/autophagy is a conserved catabolic recycling pathway in which cytoplasmic components are sequestered, degraded, and recycled to survive various stress conditions. Autophagy dysregulation has been observed and linked with the development and progression of several pathologies, including cardiovascular diseases, the leading cause of death in the developed world. In this review, we aim to provide a broad understanding of the different molecular factors that govern autophagy regulation and how these mechanisms are involved in the development of specific cardiovascular pathologies, including ischemic and reperfusion injury, myocardial infarction, cardiac hypertrophy, cardiac remodelling, and heart failure.
MeSH term(s)	Autophagy ; Cardiomegaly ; Cardiovascular Diseases/metabolism ; Heart ; Heart Failure/metabolism ; Humans
Language	English
Publishing date	2021-05-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvab158
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Article ; Online: Mitophagy in cardiovascular diseases: molecular mechanisms, pathogenesis, and treatment.

Ajoolabady, Amir / Chiong, Mario / Lavandero, Sergio / Klionsky, Daniel J / Ren, Jun

Trends in molecular medicine

2022 Volume 28, Issue 10, Page(s) 836–849

Abstract: With the growing prevalence of cardiovascular disease (CVD), there is an urgent need to explore non-conventional therapeutic measures to alleviate the burden of CVD on global healthcare. Mitochondrial injury plays a cardinal role in the pathogenesis of ... ...

Abstract	With the growing prevalence of cardiovascular disease (CVD), there is an urgent need to explore non-conventional therapeutic measures to alleviate the burden of CVD on global healthcare. Mitochondrial injury plays a cardinal role in the pathogenesis of CVD. Mitochondrial dynamics and mitophagy are essential machineries that govern mitochondrial health in cardiomyocytes in physiological and pathophysiological settings. However, with the onset and progression of CVD, homeostasis of mitophagy is disturbed through largely unknown pathological mechanisms, causing mitochondrial damage and ultimately cardiomyocyte death. In this review we decipher the dual regulatory role of mitophagy in CVD pathogenesis, summarize controversies in mitophagy, and highlight recently identified compounds capable of modulating mitophagy. We share our perspectives on future mitophagy research directions in the context of CVD.
MeSH term(s)	Cardiovascular Diseases/etiology ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/therapy ; Humans ; Mitochondria ; Mitochondrial Dynamics/physiology ; Mitophagy/physiology ; Myocytes, Cardiac/metabolism
Language	English
Publishing date	2022-07-22
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2036490-8
ISSN	1471-499X ; 1471-4914
ISSN (online)	1471-499X
ISSN	1471-4914
DOI	10.1016/j.molmed.2022.06.007
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Article: Myristate induces mitochondrial fragmentation and cardiomyocyte hypertrophy through mitochondrial E3 ubiquitin ligase MUL1.

Vásquez-Trincado, César / Navarro-Márquez, Mario / Morales, Pablo E / Westermeier, Francisco / Chiong, Mario / Parra, Valentina / Espinosa, Alejandra / Lavandero, Sergio

Frontiers in cell and developmental biology

2023 Volume 11, Page(s) 1072315

Abstract: Introduction: ...

Abstract	Introduction:
Language	English
Publishing date	2023-03-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2023.1072315
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Article ; Online: Novel Strategies to Improve the Cardioprotective Effects of Cardioplegia.

Osorio-Llanes, Estefanie / Castellar-López, Jairo / Rosales-Rada, Wendy / Montoya, Yulieth / Bustamante, John / Zalaquett, Ricardo / Bravo-Sagua, Roberto / Riquelme, Jaime A / Sánchez, Gina / Chiong, Mario / Lavandero, Sergio / Mendoza-Torres, Evelyn

Current cardiology reviews

2024

Abstract: The use of cardioprotective strategies as adjuvants of cardioplegic solutions has become an ideal alternative for the improvement of post-surgery heart recovery. The choice of the optimal cardioplegia, as well as its distribution mechanism, remains ... ...

Abstract	The use of cardioprotective strategies as adjuvants of cardioplegic solutions has become an ideal alternative for the improvement of post-surgery heart recovery. The choice of the optimal cardioplegia, as well as its distribution mechanism, remains controversial in the field of cardiovascular surgery. There is still a need to search for new and better cardioprotective methods during cardioplegic procedures. New techniques for the management of cardiovascular complications during cardioplegia have evolved with new alternatives and additives, and each new strategy provides a tool to neutralize the damage after ischemia/reperfusion events. Researchers and clinicians have committed themselves to studying the effect of new strategies and adjuvant components with the potential to improve the cardioprotective effect of cardioplegic solutions in preventing myocardial ischemia/reperfusion-induced injury during cardiac surgery. The aim of this review is to explore the different types of cardioplegia, their protection mechanisms, and which strategies have been proposed to enhance the function of these solutions in hearts exposed to cardiovascular pathologies that require surgical alternatives for their corrective progression.
Language	English
Publishing date	2024-01-24
Publishing country	United Arab Emirates
Document type	Journal Article
ISSN	1875-6557
ISSN (online)	1875-6557
DOI	10.2174/011573403X263956231129064455
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Article: Estrogen signaling as a bridge between the nucleus and mitochondria in cardiovascular diseases.

Guajardo-Correa, Emanuel / Silva-Agüero, Juan Francisco / Calle, Ximena / Chiong, Mario / Henríquez, Mauricio / García-Rivas, Gerardo / Latorre, Mauricio / Parra, Valentina

Frontiers in cell and developmental biology

2022 Volume 10, Page(s) 968373

Abstract: Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality worldwide. Epidemiological studies indicate that pre-menopausal women are more protected against the development of CVDs compared to men of the same age. This effect is ... ...

Abstract	Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality worldwide. Epidemiological studies indicate that pre-menopausal women are more protected against the development of CVDs compared to men of the same age. This effect is attributed to the action/effects of sex steroid hormones on the cardiovascular system. In this context, estrogen modulates cardiovascular function in physiological and pathological conditions, being one of the main physiological cardioprotective agents. Here we describe the common pathways and mechanisms by which estrogens modulate the retrograde and anterograde communication between the nucleus and mitochondria, highlighting the role of genomic and non-genomic pathways mediated by estrogen receptors. Additionally, we discuss the presumable role of bromodomain-containing protein 4 (BRD4) in enhancing mitochondrial biogenesis and function in different CVD models and how this protein could act as a master regulator of estrogen protective activity. Altogether, this review focuses on estrogenic control in gene expression and molecular pathways, how this activity governs nucleus-mitochondria communication, and its projection for a future generation of strategies in CVDs treatment.
Language	English
Publishing date	2022-09-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2022.968373
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Article ; Online: Regulation of total LC3 levels by angiotensin II in vascular smooth muscle cells.

Mondaca-Ruff, David / Quiroga, Clara / Norambuena-Soto, Ignacio / Riquelme, Jaime A / San Martin, Alejandra / Bustamante, Mario / Lavandero, Sergio / Chiong, Mario

Journal of cellular and molecular medicine

2022 Volume 26, Issue 5, Page(s) 1710–1713

Abstract: Hypertension is associated with high circulating angiotensin II (Ang II). We have reported that autophagy regulates Ang II-induced vascular smooth muscle cell (VSMC) hypertrophy, but the mechanism mediating this effect is still unknown. Therefore, we ... ...

Abstract	Hypertension is associated with high circulating angiotensin II (Ang II). We have reported that autophagy regulates Ang II-induced vascular smooth muscle cell (VSMC) hypertrophy, but the mechanism mediating this effect is still unknown. Therefore, we studied how Ang II regulates LC3 levels in VSMCs and whether Bag3, a co-chaperone known to regulate LC3 total levels, may be involved in the effects elicited by Ang II. A7r5 cell line or rat aortic smooth muscle cell (RASMC) primary culture were stimulated with Ang II 100 nM for 24 h and LC3 I, LC3 II and Bag3 protein levels were determined by Western blot. MAP1LC3B mRNA levels were assessed by RT-qPCR. Ang II increased MAP1LC3B mRNA levels and protein levels of LC3 I, LC3 II and total LC3 (LC3 I + LC3 II). Cycloheximide, but not actinomycin D, abolished LC3 II and total LC3 increase elicited by Ang II in RASMCs. In A7r5 cells, cycloheximide prevented the Ang II-mediated increase of LC3 I and total LC3, but not LC3 II. Moreover, Ang II increased Bag3 levels, but this increase was not observed upon co-administration with either losartan 1 μM (AT1R antagonist) or Y-27632 10 μM (ROCK inhibitor). These results suggest that Ang II may regulate total LC3 content through transcriptional and translational mechanisms. Moreover, Bag3 is increased in response to Ang II by a AT1R/ROCK signalling pathway. These data provide preliminary evidence suggesting that Ang II may stimulate autophagy in VSMCs by increasing total LC3 content and LC3 processing.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Angiotensin II/metabolism ; Angiotensin II/pharmacology ; Animals ; Apoptosis Regulatory Proteins/metabolism ; Cells, Cultured ; Cycloheximide/metabolism ; Cycloheximide/pharmacology ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Muscle, Smooth, Vascular/metabolism ; Myocytes, Smooth Muscle/metabolism ; RNA, Messenger/genetics ; Rats
Chemical Substances	Adaptor Proteins, Signal Transducing ; Apoptosis Regulatory Proteins ; BAG3 protein, rat ; LC3 protein, rat ; Microtubule-Associated Proteins ; RNA, Messenger ; Angiotensin II (11128-99-7) ; Cycloheximide (98600C0908)
Language	English
Publishing date	2022-02-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/jcmm.17215
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Article ; Online: Angiotensin-(1-9) in hypertension.

Norambuena-Soto, Ignacio / Lopez-Crisosto, Camila / Martinez-Bilbao, Javiera / Hernandez-Fuentes, Carolina / Parra, Valentina / Lavandero, Sergio / Chiong, Mario

Biochemical pharmacology

2022 Volume 203, Page(s) 115183

Abstract: Angiotensin-(1-9) [Ang-(1-9)] is a peptide of the non-canonical renin-angiotensin system (RAS) synthesized from angiotensin I by the monopeptidase angiotensin-converting enzyme type 2 (ACE2). Using osmotic minipumps, infusion of Ang-(1-9) consistently ... ...

Abstract	Angiotensin-(1-9) [Ang-(1-9)] is a peptide of the non-canonical renin-angiotensin system (RAS) synthesized from angiotensin I by the monopeptidase angiotensin-converting enzyme type 2 (ACE2). Using osmotic minipumps, infusion of Ang-(1-9) consistently reduces blood pressure in several rat hypertension models. In these animals, hypertension-induced end-organ damage is also decreased. Several pieces of evidence suggest that Ang-(1-9) is the endogenous ligand that binds and activates the type-2 angiotensin II receptor (AT2R). Activation of AT2R triggers different tissue-specific signaling pathways. This phenomenon could be explained by the ability of AT2R to form different heterodimers with other G protein-coupled receptors. Because of the antihypertensive and protective effects of AT2R activation by Ang-(1-9), associated with a short half-life of RAS peptides, several synthetic AT2R agonists have been synthesized and assayed. Some of them, particularly CGP42112, C21 and novokinin, have demonstrated antihypertensive properties. Only two synthetic AT2R agonists, C21 and LP2-3, have been tested in clinical trials, but none of them like an antihypertensive. Therefore, Ang-(1-9) is a promising antihypertensive drug that reduces hypertension-induced end-organ damage. However, further research is required to translate this finding successfully to the clinic.
MeSH term(s)	Angiotensin I/metabolism ; Angiotensin I/pharmacology ; Angiotensin I/therapeutic use ; Angiotensin II/metabolism ; Animals ; Antihypertensive Agents/pharmacology ; Antihypertensive Agents/therapeutic use ; Hypertension/drug therapy ; Imidazoles ; Peptidyl-Dipeptidase A/metabolism ; Rats ; Receptor, Angiotensin, Type 1/metabolism ; Receptor, Angiotensin, Type 2/agonists ; Renin-Angiotensin System ; Sulfonamides ; Thiophenes
Chemical Substances	Antihypertensive Agents ; Imidazoles ; Receptor, Angiotensin, Type 1 ; Receptor, Angiotensin, Type 2 ; Sulfonamides ; Thiophenes ; Angiotensin II (11128-99-7) ; Angiotensin I (9041-90-1) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; compound 21 (RC2V4W0EYC)
Language	English
Publishing date	2022-07-21
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2022.115183
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Article ; Online: Exercise regulation of hepatic lipid droplet metabolism.

Pino-de la Fuente, Francisco / Bórquez, Juan Carlos / Díaz-Castro, Francisco / Espinosa, Alejandra / Chiong, Mario / Troncoso, Rodrigo

Life sciences

2022 Volume 298, Page(s) 120522

Abstract: Lipid droplets (LD) are not just lipid stores. They are now recognized as highly dynamic organelles, having a life cycle that includes biogenesis, growth, steady-state, transport, and catabolism. Importantly, LD exhibit different features in terms of ... ...

Abstract	Lipid droplets (LD) are not just lipid stores. They are now recognized as highly dynamic organelles, having a life cycle that includes biogenesis, growth, steady-state, transport, and catabolism. Importantly, LD exhibit different features in terms of size, number, lipid composition, proteins, and interaction with other organelles, and all these features exert an impact on cellular homeostasis. The imbalance of LD function causes non-alcoholic fatty liver disease (NAFLD). Studies show that exercise attenuates NAFLD by decreasing LD content; however, reports show metabolic benefits without changes in LD amount (intrahepatic triglyceride levels) in NAFLD. Due to the multiple effects of exercise in LD features, we think that these metabolic benefits occur through changes in LD features in NAFLD, rather than only the reduction in content. Exercise increases energy mobilization and utilization from storages such as LD, and is one of the non-pharmacological treatments against NAFLD. Therefore, exercise modification of LD could be a target for NAFLD treatment. Here, we review the most up-to-date literature on this topic, and focus on recent findings showing that LD features could play an important role in the severity of NAFLD.
MeSH term(s)	Humans ; Lipid Droplets/metabolism ; Lipid Metabolism ; Lipids ; Liver/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Non-alcoholic Fatty Liver Disease/therapy
Chemical Substances	Lipids
Language	English
Publishing date	2022-03-30
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2022.120522
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