Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive lung disease characterized by abnormal epithelial repair, persistent inflammation, and excessive extracellular matrix deposition, leading to irreversible scarring and respiratory failure. Central to its pathogenesis is the dysregulation of the PI3K/Akt signaling pathway, which drives fibroblast activation, epithelial-mesenchymal transition, apoptosis resistance, and cellular senescence. Senescent cells contribute to fibrosis through the secretion of pro-inflammatory and profibrotic factors in the senescence-associated secretory phenotype (SASP). Current antifibrotic therapies, Nintedanib and Pirfenidone, only slow disease progression and are limited by side effects, highlighting the need for novel treatments. This review focuses on the role of PI3K/Akt signaling in IPF pathogenesis, its intersection with inflammation and fibrosis, and emerging therapeutic approaches targeting molecules along this pathway.

Over the last fifteen years, with the approval of the first molecular treatments, a breakthrough era has begun for patients with cystic fibrosis (CF), the rare genetic disease caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). These molecules, known as CFTR modulators, have led to unprecedented improvements in the lung function and quality of life of most CF patients. However, the efficacy of these drugs is still suboptimal, and the clinical response is highly variable even among individuals bearing the same mutation. Furthermore, not all patients carrying rare CFTR mutations are eligible for CFTR modulator therapies, indicating the need for alternative and/or add-on therapeutic approaches. Because the second messenger 3′,5′-cyclic adenosine monophosphate (cAMP) represents the primary trigger for CFTR activation and a major regulator of different steps of the life cycle of the channel, there is growing interest in devising ways to fine-tune the cAMP signaling pathway for therapeutic purposes. This review article summarizes current knowledge regarding the role of cAMP signalosomes, i.e., multiprotein complexes bringing together key enzymes of the cAMP pathway, in the regulation of CFTR function, and discusses how modulating this signaling cascade could be leveraged for therapeutic intervention in CF.

A pre-impoundment study of biotic communities was conducted in the Kishanganga river in Jammu and Kashmir on which a hydro-electric project is proposed. The present study was carried out in two phases, monsoon and post-monsoon, at three sites for the physical, chemical and biological characteristics of the river. There were no significant differences between two phases in the physical and chemical characteristics of the river water except water current velocity and turbidity. Among the biological components, significant differences were observed in the density of phytoplankton and macro-invertebrates between the two phases. Higher densities of these communities were observed during second phase with the exception of one site. Phytobenthos showed only a slight difference in the density between two phases. Didymosphenia geminata (Lyngbye) M. Schmidt. was the most common and abundant species in the phytoplankton as well as phytobenthic communities during both the phases, whereas Leptoceridae and Baetidae were the most commonly represented taxa among macro-invertebrates. Our studies suggest that the river is unpolluted and supports a rich and diverse community composed of species that are mainly pollution intolerant. This study provides baseline data for the aquatic biodiversity of an unregulated Himalayan river and for preparation of an environment management plan for conserving the biotic communities of the river.