Daniel Lagos
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Disease-causing MFN2 mutants impair mitochondrial fission dynamics by distinct DRP1 dysregulation Open
Mitochondria undergo fusion and fission. While DRP1 regulates fission, fusion is controlled by OPA1, MFN1, and MFN2. The balance between these processes and the crosstalk between machineries remains poorly understood. MFN2 mutations cause …
Mitochondrial DNA heteroplasmy drives cortical neuronal disturbances in human organoids harbouring the common m.3243A>G mutation Open
SUMMARY Mitochondrial diseases frequently affect the brain leading to severe and disabling neurological symptoms. The heteroplasmic m.3243A>G mutation in MT-TL1 , encoding mt-tRNA Leu , is responsible for ∼80% of mitochondrial encephalomyo…
View article: Mitochondrial leakage and mtDNA damage trigger early immune response in Inclusion Body Myositis
Mitochondrial leakage and mtDNA damage trigger early immune response in Inclusion Body Myositis Open
Polymyositis with mitochondrial pathology (PM-Mito) was first identified in 1997 as a subtype of idiopathic inflammatory myopathy. Recent findings demonstrated significant molecular similarities between PM-Mito and Inclusion Body Myositis …
View article: <i>OPA1</i>and disease-causing mutants perturb mitochondrial nucleoid distribution
<i>OPA1</i>and disease-causing mutants perturb mitochondrial nucleoid distribution Open
Optic atrophy protein 1 (OPA1) mediates inner mitochondrial membrane (IMM) fusion and cristae organization. Mutations in OPA1 cause autosomal dominant optic atrophy (ADOA), a leading cause of blindness. Cells from ADOA patients show impair…
Optimization of landfill gas generation based on a modified first-order decay model: a case study in the province of Quebec, Canada Open
Landfills will likely remain an essential part of integrated solid waste management systems in many developed and developing countries for the foreseeable future. Further improvements are required to model the generated gas from landfills.…
View article: <i>OPA1</i> disease-causing mutants have domain-specific effects on mitochondrial ultrastructure and fusion
<i>OPA1</i> disease-causing mutants have domain-specific effects on mitochondrial ultrastructure and fusion Open
Inner mitochondrial membrane fusion and cristae shape depend on optic atrophy protein 1, OPA1. Mutations in OPA1 lead to autosomal dominant optic atrophy (ADOA), an important cause of inherited blindness. The Guanosin Triphosphatase (GTPas…
Optimization of landfill gas generation based on a modified first-order decay model: A case study in Quebec province Open
Landfills will likely remain an essential part of integrated solid waste management systems in many developed and developing countries for the foreseeable future. This paper uses a genetic algorithm to fit parameters to a CH 4 and H 2 S ge…
Inner mitochondrial membrane structure and fusion dynamics are altered in senescent human iPSC-derived and primary rat cardiomyocytes Open
Dysfunction of the aging heart is a major cause of death in the human population. Amongst other tasks, mitochondria are pivotal to supply the working heart with ATP. The mitochondrial inner membrane (IMM) ultrastructure is tailored to meet…
View article: OPA1 Modulates Mitochondrial Ca2+ Uptake Through ER-Mitochondria Coupling
OPA1 Modulates Mitochondrial Ca2+ Uptake Through ER-Mitochondria Coupling Open
Autosomal Dominant Optic Atrophy (ADOA), a disease that causes blindness and other neurological disorders, is linked to OPA1 mutations. OPA1, dependent on its GTPase and GED domains, governs inner mitochondrial membrane (IMM) fusion and cr…
Classic and Novel Sex Hormone Binding Globulin Effects on the Cardiovascular System in Men Open
In men, 70% of circulating testosterone binds with high affinity to plasma sex hormone binding globulin (SHBG), which determines its bioavailability in their target cells. In recent years, a growing body of evidence has shown that circulat…
GDF11 Modulates Ca2+-Dependent Smad2/3 Signaling to Prevent Cardiomyocyte Hypertrophy Open
Growth differentiation factor 11 (GDF11), a member of the transforming growth factor-β family, has been shown to act as a negative regulator in cardiac hypertrophy. Ca2+ signaling modulates cardiomyocyte growth; however, the role of Ca2+-d…
Ca2+/Calmodulin-Dependent Protein Kinase II and Androgen Signaling Pathways Modulate MEF2 Activity in Testosterone-Induced Cardiac Myocyte Hypertrophy Open
Testosterone is known to induce cardiac hypertrophy through androgen receptor (AR)-dependent and -independent pathways, but the molecular underpinnings of the androgen action remain poorly understood. Previous work has shown that Ca2+/calm…
GSK-3β/NFAT Signaling Is Involved in Testosterone-Induced Cardiac Myocyte Hypertrophy Open
Testosterone induces cardiac hypertrophy through a mechanism that involves a concerted crosstalk between cytosolic and nuclear signaling pathways. Nuclear factor of activated T-cells (NFAT) is associated with the promotion of cardiac hyper…