Climate change is a reality, and poses a serious long term threat to society and to the environment. Much has been written on the negative effects of climate change across the globe focusing on the greater vulnerability of least developed countries and developing countries. Numerous studies back up the argument that “countries that are most vulnerable to the effects of climate change tend to be poorer with a wider gender gap. In contrast, countries that rank high in environmental performance and gender equality, are among the richest nations of the world” (Samy, 2011, p. 100). Women are often denied of their basic rights due to discriminatory social practices and gender blind policies. Impacts of climate change affect life and livelihood of women, and diverse work responsibilities of women augment their exposure to climate hazards. Due to less access or rights to financial and productive resources, information and services that may help them cope with impacts of stresses and shocks, are not present as a result of the gaps in policies, development agendas, thus leaving women in a greater vulnerable condition. Primarily, these are the reasons slowing the progress on achieving overall gender equality. The objective of this paper is to look at the Post 2015 Arrangements. These are numerous international frameworks and agreements ie SFDRR, SDG and the Paris Agreement, that will determine sustainable development for humanitarian response and climate politics as well as policies for the next fifteen years. They focus on development from a climate change and gender equality point of view, in particular how the policies are enabling ‘gender equality', taking common but differentiated responsibilities, and equity, justice and fairness as principles.
Climate change is a reality, and poses a serious long term threat to society and to the environment. Much has been written on the negative effects of climate change across the globe focusing on the greater vulnerability of least developed countries and developing countries. Numerous studies back up the argument that “countries that are most vulnerable to the effects of climate change tend to be poorer with a wider gender gap. In contrast, countries that rank high in environmental performance and gender equality, are among the richest nations of the world” (Samy, 2011, p. 100). Women are often denied of their basic rights due to discriminatory social practices and gender blind policies. Impacts of climate change affect life and livelihood of women, and diverse work responsibilities of women augment their exposure to climate hazards. Due to less access or rights to financial and productive resources, information and services that may help them cope with impacts of stresses and shocks, are not present as a result of the gaps in policies, development agendas, thus leaving women in a greater vulnerable condition. Primarily, these are the reasons slowing the progress on achieving overall gender equality. The objective of this paper is to look at the Post 2015 Arrangements. These are numerous international frameworks and agreements ie SFDRR, SDG and the Paris Agreement, that will determine sustainable development for humanitarian response and climate politics as well as policies for the next fifteen years. They focus on development from a climate change and gender equality point of view, in particular how the policies are enabling ‘gender equality', taking common but differentiated responsibilities, and equity, justice and fairness as principles.
Pathological deposition and crosslinking of collagen type I by activated myofibroblasts drives progressive tissue fibrosis. Therapies that inhibit collagen synthesis by myofibroblasts have clinical potential as anti-fibrotic agents. Lysine hydroxylation by the prolyl-3-hydroxylase complex, comprised of cartilage associated protein, prolyl 3-hydroxylase 1, and cyclophilin B, is essential for collagen type I crosslinking and formation of stable fibers. Here, we identify the collagen chaperone cyclophilin B as a major cellular target of the macrocyclic natural product sanglifehrin A (SfA) using photo-affinity labeling and chemical proteomics. Our studies reveal a unique mechanism of action in which SfA binding to cyclophilin B in the endoplasmic reticulum (ER) induces the secretion of cyclophilin B to the extracellular space, preventing TGF-β-activated myofibroblasts from synthesizing collagen type I in vitro without inhibiting collagen type I mRNA transcription or inducing ER stress. In addition, SfA prevents collagen type I secretion without affecting myofibroblast contractility or TGF-β1 signaling. In vivo, we provide chemical, molecular, functional, and translational evidence that SfA mitigates the development of lung and skin fibrosis in mouse models by inducing cyclophilin B secretion, thereby inhibiting collagen synthesis from fibrotic fibroblasts in vivo. Consistent with these findings in preclinical models, SfA reduces collagen type I secretion from fibrotic human lung fibroblasts and precision cut lung slices from patients with idiopathic pulmonary fibrosis, a fatal fibrotic lung disease with limited therapeutic options. Our results identify the primary liganded target of SfA in cells, the collagen chaperone cyclophilin B, as a new mechanistic target for the treatment of organ fibrosis.
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