This study investigates the impact of financial inclusion on environmental sustainability in 178 emerging and developing countries from 1996 to 2022. Employing a composite index derived through Principal Component Analysis (PCA) as a measure of financial inclusion and covering four aspects (access, depth, efficiency, stability), our analysis reveals negative outcomes. The findings indicate that enhancing financial inclusion is associated with a notable increase in CO2 per capita emissions as well as in Total Greenhouse Gas emissions. We demonstrate that controlling corruption improves environmental quality, yet this measure alone is insufficient to fully mitigate the impact of financial inclusion, as indicated by our moderation analysis. The same analysis, however, shows that fostering globalization through trade openness is an efficient tool to alleviate the positive effect of financial inclusion on the quality of the environment. The study employs various policies targeting the control of development levels, energy consumption, natural resource utilization, industry, and urban population dynamics to contextualize the influence of financial inclusion on environmental sustainability. Through econometric methods and a comprehensive examination of the specified time frame, our results provide insights into the complex interplay between financial inclusion and environmental outcomes in diverse socio-economic contexts. The research contributes to the discourse on sustainable development by highlighting the potential of certain factors as a catalyst for environmental improvement. Understanding these dynamics is crucial for policymakers, as it underlines the trade-off between integrating inclusive financial strategies and achieving environmentally sustainable development trajectories in emerging and developing nations. Moreover, shedding light on the underlying mechanisms, such as trade-offs, fills a significant gap in the literature.

The answer to how to stop economic growth must be political rather than economic. Economic growth made by men has an impetus which can only be stopped by a deliberate choice. It takes national and international decisions to stop it. In order to organize a moratorium on economic growth (which eventually must lead to a stop on growth) I suggest to create blocks of nations in the world. The European Union can function as a model for such a block. The E.U. is on its way of becoming a supra-national government which was created to ensure a level playing field for its members. Now it is meant to create economic growth for its members, in the future its administration should be used to stop it. Blocks should agree on the targets to reach a durable economy. Globally or between certain more advanced blocks a date should be set to stop economic growth after that date. Each block should implement the goals to reach a durable economy and prevent products reaching its market that violate the goals of durability. Blocks in developing countries cannot be expected to stop economic growth. They need that growth for two reasons. Eventually they must reach the level of existence in the more advanced block and secondly they must have the time to improve the standard for durability of their products. They need the aid of the developed countries to reach a higher but also more durable level of production, but this aid comes with a quid pro quo, In the meantime they must do their utmost to stop wars in their regions and conduct a responsible population-policy to reduce the growth of their population and let it reduce on the long term.

The latent transforming growth factor-beta (TGF-β) binding protein 1 (LTBP1) has been implicated in various cellular processes, but its role in triple-negative breast cancer (TNBC) remains unclear. In this study, we investigated the impact of LTBP1 on TNBC progression and its underlying mechanisms. Analysis of online datasets revealed elevated LTBP1 mRNA expression in breast cancer tissues compared to normal adjacent tissues. Kaplan-Meier Plotter analysis indicated that high LTBP1 expression was negatively correlated with relapse-free survival (RFS), distant-metastasis free survival (DMFS), and overall survival (OS) of breast cancer patients. Additionally, LTBP1 mRNA levels were associated with chemotherapy resistance. Functional assays in TNBC cells demonstrated that LTBP1 knockdown suppressed cell proliferation, induced apoptosis, and attenuated migration and invasion. In vivo studies confirmed that LTBP1 knockdown inhibited tumor growth in a xenograft mouse model. Mechanistically, LTBP1 positively correlated with genes involved in signaling regulation and organelle organization, with significant associations to GTPase binding and the RhoA/ROCK pathway. LTBP1 knockdown reduced RhoA activity and phosphorylation of Myosin Light Chain 2 (MLC2), suggesting inhibition of the RhoA/ROCK signaling pathway. Moreover, activation of the RhoA/ROCK pathway partially rescued the effects of LTBP1 knockdown on TNBC cell proliferation, apoptosis, migration, and invasion. In conclusion, our findings suggest that LTBP1 promotes TNBC progression through activation of the RhoA/ROCK signaling pathway, highlighting its potential as a therapeutic target for TNBC.