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Article: Unraveling the role of galectin-3 in cardiac pathology and physiology.

Seropian, Ignacio M / Cassaglia, Pablo / Miksztowicz, Verónica / González, Germán E

2023 Volume 14, Page(s) 1304735

Abstract: Galectin-3 (Gal-3) is a carbohydrate-binding protein with multiple functions. Gal-3 regulates cell growth, proliferation, and apoptosis by orchestrating cell-cell and cell-matrix interactions. It is implicated in the development and progression of ... ...

Abstract	Galectin-3 (Gal-3) is a carbohydrate-binding protein with multiple functions. Gal-3 regulates cell growth, proliferation, and apoptosis by orchestrating cell-cell and cell-matrix interactions. It is implicated in the development and progression of cardiovascular disease, and its expression is increased in patients with heart failure. In atherosclerosis, Gal-3 promotes monocyte recruitment to the arterial wall boosting inflammation and atheroma. In acute myocardial infarction (AMI), the expression of Gal-3 increases in infarcted and remote zones from the beginning of AMI, and plays a critical role in macrophage infiltration, differentiation to M1 phenotype, inflammation and interstitial fibrosis through collagen synthesis. Genetic deficiency of Gal-3 delays wound healing, impairs cardiac remodeling and function after AMI. On the contrary, Gal-3 deficiency shows opposite results with improved remodeling and function in other cardiomyopathies and in hypertension. Pharmacologic inhibition with non-selective inhibitors is also protective in cardiac disease. Finally, we recently showed that Gal-3 participates in normal aging. However, genetic absence of Gal-3 in aged mice exacerbates pathological hypertrophy and increases fibrosis, as opposed to reduced fibrosis shown in cardiac disease. Despite some gaps in understanding its precise mechanisms of action, Gal-3 represents a potential therapeutic target for the treatment of cardiovascular diseases and the management of cardiac aging. In this review, we summarize the current knowledge regarding the role of Gal-3 in the pathophysiology of heart failure, atherosclerosis, hypertension, myocarditis, and ischemic heart disease. Furthermore, we describe the physiological role of Gal-3 in cardiac aging.
Language	English
Publishing date	2023-12-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2023.1304735
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Article ; Online: An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice.

Fontana Estevez, Florencia S / Miksztowicz, Verónica / Seropián, Ignacio M / Cassaglia, Pablo / Bustos, Romina / Touceda, Vanessa / Cianciulli, Tomas / Cassanova, Verónica / Morales, Celina / González, Germán E

Journal of visualized experiments : JoVE

2023 , Issue 197

Abstract: Cardiovascular disease is the most prevalent cause of death in Western countries, with acute myocardial infarction (MI) being the most prevalent form. This paper describes a protocol for studying the role of galectin 3 (Gal-3) in the temporal evolution ... ...

Abstract	Cardiovascular disease is the most prevalent cause of death in Western countries, with acute myocardial infarction (MI) being the most prevalent form. This paper describes a protocol for studying the role of galectin 3 (Gal-3) in the temporal evolution of cardiac healing and remodeling in an experimental animal model of MI. The procedures described include an experimental model of MI with a permanent coronary ligature in male C57BL/6J (control) and Gal-3 knockout (KO) mice, an echocardiography procedure to study cardiac remodeling and systolic function in vivo, a histological evaluation of interstitial myocardial fibrosis with picrosirius red-stained and rhodamine-conjugated lectin-stained sections for studying myocyte hypertrophy by the cross-sectional area (MCSA), and the quantification of infarct size and cardiac remodeling (scar thinning, septum thickness, and expansion index) by planimetry in slices stained with Masson's trichrome and triphenyl tetrazolium chloride. Gal-3 KO mice with MI showed disrupted cardiac remodeling and an increase in the scar thinning ratio and the expansion index. At the onset of MI, myocardial function and cardiac remodeling were also severely affected. At 4 weeks post MI, the natural evolution of fibrosis in infarcted Gal-3 KO mice was also affected. In summary, the experimental model of MI is a suitable model for studying the temporal evolution of cardiac repair and remodeling in mice with the genetic deletion of Gal-3 and other animal models. The lack of Gal-3 affects the dynamics of cardiac repair and disrupts the evolution of cardiac remodeling and function after MI.
Language	English
Publishing date	2023-07-14
Publishing country	United States
Document type	Journal Article ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/64143
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Article ; Online: Galectin-3 contributes to acute cardiac dysfunction and toxicity by increasing oxidative stress and fibrosis in doxorubicin-treated mice.

Seropian, Ignacio M / Fontana Estevez, Florencia S / Villaverde, Alejo / Cacciagiú, Leonardo / Bustos, Romina / Touceda, Vanessa / Penas, Federico / Selser, Carolina / Morales, Celina / Miksztowicz, Verónica / González, Germán E

International journal of cardiology

2023 Volume 393, Page(s) 131386

Abstract: Background: Doxorubicin (DOX) leads to cardiovascular toxicity through direct cardiomyocyte injury and inflammation. We aimed to study the role of Galectin-3 (Gal-3), a β-galactosidase binding lectin associated with inflammation and fibrosis in DOX- ... ...

Abstract	Background: Doxorubicin (DOX) leads to cardiovascular toxicity through direct cardiomyocyte injury and inflammation. We aimed to study the role of Galectin-3 (Gal-3), a β-galactosidase binding lectin associated with inflammation and fibrosis in DOX-induced acute cardiotoxicity in mice. Methods: Male C57 and Gal-3 knockout (KO) mice were given a single dose of DOX (15 mg/kg, i.p) or placebo. Serum creatine phosphokinase (CPK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST) and cardiac thiobarbituric acid-reactive substance (TBARS) were measured at 3 days to assess cardiac injury and oxidative stress. Cardiac remodeling and function were studied by echocardiography and catheterization at 7 days. Myocardial fibrosis was quantified in picrosirius red stained slices. Results: Absence of Gal-3 tended to reduce the mortality after DOX. DOX significantly increased CPK, LDH, AST and TBARS while treated Gal-3 KO mice showed reduced injury and oxidative stress. After 7 days, adverse remodeling, fibrosis and dysfunction in treated-C57 mice were severely affected while those effects were prevented by absence of Gal-3. Conclusion: In summary, genetic deletion of Gal-3 prevented cardiac damage, adverse remodeling and dysfunction, associated with reduced cardiac oxidative stress and fibrosis. Understanding the contribution of GAL-3 to doxorubicin-induced cardiac toxicity reinforces its potential use as a therapeutic target in patients with several cancer types.
MeSH term(s)	Humans ; Mice ; Male ; Animals ; Galectin 3/genetics ; Galectin 3/metabolism ; Thiobarbituric Acid Reactive Substances/adverse effects ; Thiobarbituric Acid Reactive Substances/metabolism ; Doxorubicin/toxicity ; Oxidative Stress ; Myocytes, Cardiac/metabolism ; Cardiomyopathies/metabolism ; Mice, Knockout ; Cardiotoxicity/metabolism ; Fibrosis ; Inflammation/metabolism ; Apoptosis
Chemical Substances	Galectin 3 ; Thiobarbituric Acid Reactive Substances ; Doxorubicin (80168379AG)
Language	English
Publishing date	2023-09-22
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	779519-1
ISSN	1874-1754 ; 0167-5273
ISSN (online)	1874-1754
ISSN	0167-5273
DOI	10.1016/j.ijcard.2023.131386
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Article: Cardiac Natriuretic Peptide Profiles in Chronic Hypertension by Single or Sequentially Combined Renovascular and DOCA-Salt Treatments.

Cerrudo, Carolina S / Cavallero, Susana / Rodríguez Fermepín, Martín / González, Germán E / Donato, Martín / Kouyoumdzian, Nicolás M / Gelpi, Ricardo J / Hertig, Cecilia M / Choi, Marcelo R / Fernández, Belisario E

Frontiers in physiology

2021 Volume 12, Page(s) 651246

Abstract: The involvement of natriuretic peptides was studied during the hypertrophic remodeling transition mediated by sequential exposure to chronic hemodynamic overload. We induced hypertension in rats by pressure (renovascular) or volume overload (DOCA-salt) ... ...

Abstract	The involvement of natriuretic peptides was studied during the hypertrophic remodeling transition mediated by sequential exposure to chronic hemodynamic overload. We induced hypertension in rats by pressure (renovascular) or volume overload (DOCA-salt) during 6 and 12 weeks of treatment. We also studied the consecutive combination of both models in inverse sequences: RV 6 weeks/DS 6 weeks and DS 6 weeks/RV 6 weeks. All treated groups developed hypertension. Cardiac hypertrophy and left ventricular ANP gene expression were more pronounced in single DS than in single RV groups. BNP gene expression was positively correlated with left ventricular hypertrophy only in RV groups, while ANP gene expression was positively correlated with left ventricular hypertrophy only in DS groups. Combined models exhibited intermediate values between those of single groups at 6 and 12 weeks. The latter stimulus associated to the second applied overload is less effective than the former to trigger cardiac hypertrophy and to increase ANP and BNP gene expression. In addition, we suggest a correlation of ANP synthesis with volume overload and of BNP synthesis with pressure overload-induced hypertrophy after a prolonged treatment. Volume and pressure overload may be two mechanisms, among others, involved in the differential regulation of ANP and BNP gene expression in hypertrophied left ventricles. Plasma ANP levels reflect a response to plasma volume increase and volume overload, while circulating BNP levels seem to be regulated by cardiac BNP synthesis and ventricular hypertrophy.
Language	English
Publishing date	2021-05-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2021.651246
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Article ; Online: Ludwig: the bioengineer.

Valentinuzzi, Max E / Beneke, Klaus / González, Germán E

IEEE pulse

2012 Volume 3, Issue 4, Page(s) 68–9, 72, 74–5 passim

Abstract: On the basis of the strict exclusion of the vis vitalis, the demand was raised by Carl Ludwig, Helmholtz, Du Bois-Reymond, and Brucke for a physiology which was causal-analytical and physically and chemically experimental. If, out of these four ... ...

Abstract	On the basis of the strict exclusion of the vis vitalis, the demand was raised by Carl Ludwig, Helmholtz, Du Bois-Reymond, and Brucke for a physiology which was causal-analytical and physically and chemically experimental. If, out of these four investigators, we pick Ludwig as the actual founder of modern physiology, the grounds for this must be justified specifically. That modern physiology is not to be contemplated without the works of the three great students of Johannes Muller is explicitly emphasized. However, Carl Ludwig occupies a special position for physiology.
MeSH term(s)	Animals ; Anura ; Bioengineering/history ; History, 19th Century ; Humans ; Kymography/history ; Male ; Physiology/history ; Rabbits
Language	English
Publishing date	2012-07
Publishing country	United States
Document type	Historical Article ; Journal Article
ZDB-ID	2567191-1
ISSN	2154-2317 ; 2154-2287
ISSN (online)	2154-2317
ISSN	2154-2287
DOI	10.1109/MPUL.2012.2192758
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Article ; Online: Early administration of Enalapril prevents diastolic dysfunction and ventricular remodeling in rabbits with myocardial infarction.

González, Germán E / Wilensky, Luciana / Cassaglia, Pablo / Morales, Celina / Gelpi, Ricardo J

Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology

2016 Volume 25, Issue 3, Page(s) 208–213

Abstract: We aimed to investigate the role of early administration of Enalapril (Enal) on post-myocardial infarction (MI) ventricular remodeling and diastolic dysfunction in rabbits. White New Zealand rabbits that underwent coronary artery ligature or Sham were ... ...

Abstract	We aimed to investigate the role of early administration of Enalapril (Enal) on post-myocardial infarction (MI) ventricular remodeling and diastolic dysfunction in rabbits. White New Zealand rabbits that underwent coronary artery ligature or Sham were divided in three experimental groups: (1) Sham, (2) MI, and (3) MI+Enal. Enal was given by gavage at a dose of 10mg/kg/day starting at 3h after surgery for 35days. At the end of the protocol, we measured (1) mean arterial pressure, (2) left ventricular (LV)+dP/dtmax, (3) LV end-diastolic pressure (LVEDP) and isovolumic relaxation (Tau), (4) LV dimensions, (5) LV ejection and shortening fraction, (6) infarct size (Masson's trichrome-stained slices), (7) fibrosis in the infarct and remote zone (Picrosirius red-stained slices), and (8) myocyte cross-sectional area (MCSA) in WGA-stained section. Enal reduced the mean arterial pressure by 30% as compared with untreated animals and Sham (P<.05). MI reduced LV+dP/dtmax and LV-dP/dtmax (mmHg/s), increased LVEDP (mmHg), Tau (ms), and t50 (ms) values, suggesting a decrease in the relaxation rate. LV end-diastolic dimension and LV end-systolic dimension (LVESD, mm) increased in untreated MI (P<.05 vs. Sham). In contrast, Enal markedly prevented post-MI diastolic dysfunction by significantly decrease LVEDP from 8.2±0.2 to 5.1±0.3mmHg, Tau from 19.8±0.8 to 15.3±0.9ms, and t50 from 12.4±0.5 to 9.6±0.8ms as well as reduced LVESD from 15±1.1 to 12±0.8mm (P<.05 MI vs. MI+Enal). Collagen concentration in the scar was unaffected, but chronic treatment with Enal prevented myocardial fibrosis and MCSA in the remote zone. In summary, chronic early administration of Enal to rabbits with experimental MI has a favorable effect on ventricular remodeling and diastolic function by reducing MCSA and fibrosis, without affecting the wound healing.
MeSH term(s)	Angiotensin-Converting Enzyme Inhibitors/pharmacology ; Animals ; Diastole/drug effects ; Enalapril/pharmacology ; Fibrosis/pathology ; Heart/drug effects ; Myocardial Infarction/pathology ; Myocardium/pathology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/pathology ; Rabbits ; Random Allocation ; Ventricular Remodeling/drug effects
Chemical Substances	Angiotensin-Converting Enzyme Inhibitors ; Enalapril (69PN84IO1A)
Language	English
Publishing date	2016-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	1134600-0
ISSN	1879-1336 ; 1054-8807
ISSN (online)	1879-1336
ISSN	1054-8807
DOI	10.1016/j.carpath.2016.01.004
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Article ; Online: Galectin-1 as an Emerging Mediator of Cardiovascular Inflammation: Mechanisms and Therapeutic Opportunities.

Seropian, Ignacio M / González, Germán E / Maller, Sebastián M / Berrocal, Daniel H / Abbate, Antonio / Rabinovich, Gabriel A

Mediators of inflammation

2018 Volume 2018, Page(s) 8696543

Abstract: Galectin-1 (Gal-1), an evolutionarily ... ...

Abstract	Galectin-1 (Gal-1), an evolutionarily conserved
MeSH term(s)	Animals ; Galectin 1/metabolism ; Homeostasis/physiology ; Humans ; Inflammation/metabolism ; T-Lymphocytes, Regulatory/metabolism ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Galectin 1 ; Vascular Endothelial Growth Factor A
Language	English
Publishing date	2018-11-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1137605-3
ISSN	1466-1861 ; 0962-9351
ISSN (online)	1466-1861
ISSN	0962-9351
DOI	10.1155/2018/8696543
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Article ; Online: The allometric model in chronic myocardial infarction

Bonomini Maria P / Arini Pedro D / Gonzalez Germán E / Buchholz Bruno / Valentinuzzi Max E

Theoretical Biology and Medical Modelling, Vol 9, Iss 1, p

2012 Volume 15

Abstract: Abstract Background An allometric relationship between different electrocardiogram (ECG) parameters and infarcted ventricular mass was assessed in a myocardial infarction (MI) model in New Zealand rabbits. Methods A total of fifteen animals were used, ... ...

Abstract	Abstract Background An allometric relationship between different electrocardiogram (ECG) parameters and infarcted ventricular mass was assessed in a myocardial infarction (MI) model in New Zealand rabbits. Methods A total of fifteen animals were used, out of which ten underwent left anterior descending coronary artery ligation to induce infarction (7–35% area). Myocardial infarction (MI) evolved and stabilized during a three month-period, after which, rabbits were sacrificed and the injured area was histologically confirmed. Right before sacrifice, ECGs were obtained to correlate several of its parameters to the infarcted mass. The latter was normalized after combining data from planimetry measurements and heart weight. The following ECG parameters were studied: RR and PR intervals, P-wave duration (P D ), QRS duration (QRS D ) and amplitude (QRS A ), Q-wave (Q A ), R-wave (R A ) and S-wave (S A ) amplitudes, T-wave peak amplitude (T A ), the interval from the peak to the end of the T-wave (T PE ), ST-segment deviation (ST A ), QT interval (QT), corrected QT and JT intervals. Corrected QT was analyzed with different correction formulae, i.e., Bazett (QT B ), Framingham (QT FRA ), Fridericia (QT FRI ), Hodge (QT HO ) and Matsunaga (QT MA ) and compared thereafter. The former variables and infarcted ventricular mass were then fitted to the allometric equation in terms of deviation from normality, in turn derived after ECGs in 5 healthy rabbits. Results Six variables (JT, QT B , Q A , S A , T A and ST A ) presented statistical differences among leads. QT showed the best allometric fit ( r = 0.78), followed by T A ( r = 0.77), ST A ( r = 0.75), QT FRA ( r = 0.72), T PE ( r = 0.69), QT FRI ( r = 0.68) and QT MA ( r = 0.68). Corrected QT’s (QT FRA , QT FRI and QT MA ) performed worse than the uncorrected counterpart (QT), the former scaling allometrically with similar goodness of fits. Conclusions QT, T A , ST A and T PE could possibly be used to assess infarction extent in an old MI event through the allometric model as a first approach. Moreover, the T PE also produced a good allometric scaling, leading to the potential existence of promising allometric indexes to diagnose malignant arrhythmias.
Keywords	Allometric law ; ECG parameters ; Chronic infarction extent ; Myocardial infarction model ; Computer applications to medicine. Medical informatics ; R858-859.7 ; Biology (General) ; QH301-705.5
Subject code	290
Language	English
Publishing date	2012-05-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Effects of third-generation β-blockers, atenolol or amlodipine on blood pressure variability and target organ damage in spontaneously hypertensive rats.

Del Mauro, Julieta S / Prince, Paula D / Allo, Miguel A / Santander Plantamura, Yanina / Morettón, Marcela A / González, Germán E / Bertera, Facundo M / Carranza, Andrea / Gorzalczany, Susana B / Chiappetta, Diego A / Morales, Celina / Gelpi, Ricardo J / Taira, Carlos A / Polizio, Ariel H / Donato, Martín / Höcht, Christian

Journal of hypertension

2020 Volume 38, Issue 3, Page(s) 536–545

Abstract: Background: β-blockers are no longer considered as first-line antihypertensive drugs due to their lower cardioprotection.: Method: Considering the differences in the pharmacological properties of β-blockers, the present work compared the effects of ... ...

Abstract	Background: β-blockers are no longer considered as first-line antihypertensive drugs due to their lower cardioprotection. Method: Considering the differences in the pharmacological properties of β-blockers, the present work compared the effects of third-generation β-blockers - carvedilol and nebivolol - with a first-line agent - amlodipine - on hemodynamic parameters, including short-term blood pressure variability (BPV), and their ability to prevent target organ damage in spontaneously hypertensive rats (SHR). SHR rats were orally treated with carvedilol, nebivolol, atenolol, amlodipine or vehicle for 8 weeks. Wistar Kyoto rats treated with vehicle were used as normotensive group. Echocardiographic evaluation, BP, and short-term BPV measurements were performed. Left ventricle and thoracic aorta were removed for histological evaluations and to assess the expression of transforming growth factor β (TGF-β), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Results: Carvedilol, nebivolol or amlodipine induced a greater reduction of carotid BP, short-term BPV and echocardiography parameters than atenolol in SHR rats. Carvedilol, nebivolol and amlodipine were more effective than atenolol in the prevention of cardiac hypertrophy, and cardiac and aortic collagen deposit. Carvedilol and nebivolol, but not atenolol, reduced the expressions of fibrotic and inflammatory biomarkers - TGF-β, TNF-α and IL-6 - in SHR rats to a similar extent to that of amlodipine. Conclusion: Chronic treatment with carvedilol or nebivolol attenuates carotid BP and short-term BPV, and reduces target organ damage in SHR to a greater extent than atenolol. Our findings suggest that the lower cardiovascular protection of nonvasodilating β-blockers, as atenolol, in hypertension must not be translated to third-generation β-blockers.
MeSH term(s)	Adrenergic beta-Antagonists/adverse effects ; Adrenergic beta-Antagonists/pharmacology ; Amlodipine/adverse effects ; Amlodipine/pharmacology ; Animals ; Antihypertensive Agents/pharmacology ; Aorta/drug effects ; Atenolol/adverse effects ; Atenolol/pharmacology ; Blood Pressure/drug effects ; Cytokines/metabolism ; Heart Ventricles/drug effects ; Rats ; Rats, Inbred SHR
Chemical Substances	Adrenergic beta-Antagonists ; Antihypertensive Agents ; Cytokines ; Amlodipine (1J444QC288) ; Atenolol (50VV3VW0TI)
Language	English
Publishing date	2020-02-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605532-1
ISSN	1473-5598 ; 0263-6352 ; 0952-1178
ISSN (online)	1473-5598
ISSN	0263-6352 ; 0952-1178
DOI	10.1097/HJH.0000000000002284
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Article ; Online: Genetic Deletion of Galectin-3 Alters the Temporal Evolution of Macrophage Infiltration and Healing Affecting the Cardiac Remodeling and Function after Myocardial Infarction in Mice.

Cassaglia, Pablo / Penas, Federico / Betazza, Celeste / Fontana Estevez, Florencia / Miksztowicz, Verónica / Martínez Naya, Nadia / Llamosas, María Clara / Noli Truant, Sofía / Wilensky, Luciana / Volberg, Verónica / Cevey, Ágata C / Touceda, Vanessa / Cicale, Eliana / Berg, Gabriela / Fernández, Marisa / Goren, Nora / Morales, Celina / González, Germán E

The American journal of pathology

2020 Volume 190, Issue 9, Page(s) 1789–1800

Abstract: We studied the role of galectin-3 (Gal-3) in the expression of alternative activation markers (M2) on macrophage, cytokines, and fibrosis through the temporal evolution of healing, ventricular remodeling, and function after myocardial infarction (MI). ... ...

Abstract	We studied the role of galectin-3 (Gal-3) in the expression of alternative activation markers (M2) on macrophage, cytokines, and fibrosis through the temporal evolution of healing, ventricular remodeling, and function after myocardial infarction (MI). C57BL/6J and Gal-3 knockout mice (Lgals3
MeSH term(s)	Animals ; Galectin 3/metabolism ; Macrophages/metabolism ; Macrophages/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Ventricular Remodeling/physiology ; Wound Healing/physiology
Chemical Substances	Galectin 3
Language	English
Publishing date	2020-05-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2020.05.010
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