Krt5, also known as keratin 5, is a key intermediate filament protein. It is involved in maintaining the structural integrity of epithelial cells and is associated with multiple biological processes. In the context of signaling pathways, it has been linked to the Notch signaling pathway, which is crucial for cell-cell communication, differentiation, and development [4].

In the lung, Krt5-related research has shown significant findings. In idiopathic pulmonary fibrosis (IPF), the extracellular matrix (ECM) modulates Krt5+ basal cell activity. Changes in ECM composition, like over-expression of SPARC in IPF lung fibroblasts, restrict Krt5+ cell migration in vitro, influencing remodelling events in the fibrotic niche [1]. Also, human alveolar type 2 cells can transdifferentiate into metaplastic Krt5+ basal cells in response to fibrotic signalling in the lung mesenchyme, both in vitro and in vivo [2]. Moreover, p63(+)Krt5(+) distal airway stem cells are essential for lung regeneration. Ablation of these cells in vivo prevents lung regeneration after influenza-induced damage, leading to pre-fibrotic lesions and deficient oxygen exchange [3].

In melanoma, knockdown of Krt5 promoted the proliferation, migration, and invasion of A375 cells, indicating its inhibitory role in melanoma metastasis [5].

In the kidney, Krt5+ urothelial cells act as developmental and tissue repair progenitors, differentiating into Upk+ RUCs during normal ontogeny and after congenital urinary tract obstruction (UTO) [6].

In conclusion, Krt5 is essential for maintaining epithelial integrity and is involved in various biological processes such as cell differentiation, tissue regeneration, and response to disease. Studies, especially those using in vivo models like gene-knockout mouse models, have revealed its significance in diseases including pulmonary fibrosis, melanoma, and kidney obstructive nephropathy. Understanding Krt5 provides insights into disease mechanisms and potential therapeutic targets.