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Using carbon dioxide (CO2) as a raw-material to produce value-added chemicals has a strategic role to play in the decarbonization of energy resources and the transition to a climate-neutral economy. E-methanol, Synthetic Natural Gas (SNG) and e-kerosene are one of the most promising pathways to convert CO2. In this context, the aim of this work is to propose an optimized and integrated CO2 to methanol process and then to compare it to the CO2 to SNG process from economic and environmental points of views. An optimized reactor configuration in the CO2 to methanol conversion unit has been successfully implemented in Aspen Plus® and leads to a thermal energy self-sufficiency of this unit. A heat integration with an advanced capture unit has been performed where 5 % of the heat requirement could be provided from the conversion unit while 95 % come from external steam source. Techno-economic assessment of the optimized process showed that methanol is more profitable when it is used as a raw material to synthetize other chemicals. As an energy carrier, SNG is more interesting. Compared to the reference scenario, a net CO2 emission reduction of 70 % in the CO2 to SNG route and of 60 % in the CO2 to methanol route were obtained. Concerning the fossil depletion impact, in both cases, a reduction of more than 60 % was noticed (ca. 75 % in CO2 to SNG route and 61 % in CO2 to methanol case).

Cardiac fibrosis is a severe outcome of Chagas disease (CD), caused by the protozoan Trypanosoma cruzi. Clinical evidence revealed a correlation between fibrosis levels with impaired cardiac performance in CD patients. Therefore, we sought to analyze the effect of inhibitors of TGF-β (pirfenidone), p38-MAPK (losmapimod) and c-Jun (SP600125) on the modulation of collagen deposition in cardiac fibroblasts (CF) and in vivo models of T. cruzi chronic infection. Sirius Red/Fast Green dye was used to quantify both collagen expression and total protein amount, assessing cytotoxicity. The compounds were also used to treat C57/Bl6 mice chronically infected with T. cruzi, Brazil strain. We identified an anti-fibrotic effect in vitro for pirfenidone (TGF-β inhibitor, IC50 114.3 μM), losmapimod (p38 inhibitor, IC50 17.6 μM) and SP600125 (c-Jun inhibitor, IC50 3.9 μM). This effect was independent of CF proliferation since these compounds do not affect T. cruzi-induced host cell multiplication as measured by BrdU incorporation. Assays of chronic infection of mice with T. cruzi have shown a reduction in heart collagen by pirfenidone. These results propose a novel approach to fibrosis therapy in CD, with the prospect of repurposing pirfenidone to prevent the onset of ECM accumulation in the hearts of the patients.