Ana Esther Estrada Rodriguez

The kidneys contribute to the overall health of an organism by maintaining systemic homeostasis. This process involves various biological mechanisms, in which the Krüppel-like factors (KLFs), a family of transcription factors, are essential for regulating development, differentiation, proliferation, and cellular apoptosis. They also play a role in the metabolic regulation of essential nutrients, such as glucose and lipids. The dysregulation of these transcription factors is associated with the development of various pathologies, which can ultimately lead to renal fibrosis, severely compromising kidney function. In this context, the present article provides a comprehensive review of the existing literature, offering an enriching analysis of the findings related to the role of KLFs in nephrology, while also highlighting their potential therapeutic role in the treatment of renal diseases.

The kidneys contribute to the overall health of the organism by maintaining systemic homeostasis. This process involves the regulation of various biological mechanisms, in which the Krüppel-like factor (KLF) transcription factors are essential for regulating development, differentiation, proliferation, and cellular apoptosis. They also play a role in the metabolic regulation of essential nutrients, such as glucose and lipids. The dysregulation of these transcription factors is associated with the development of various pathologies, which can ultimately lead to renal fibrosis, a process that severely compromises the function of these organs. In this context, the present article provides a comprehensive review of the existing literature, offering an enriching analysis of the findings related to the role of KLFs in the renal field, while also highlighting their potential therapeutic role in the treatment of renal diseases.

Cardiac hypertrophy typically follows myocardial damage, a process known to involve members of the Krüppel-Like Factors (KLFs) which have pro-hypertrophic and anti-hypertrophic roles. Our study delved into the molecular mechanisms underlying KLFs-cardiac hypertrophy interplay post myocardial infraction. We induced myocardial dam-age in rats using isoproterenol. Total RNA was extracted from the left ventricle and Quantitative Real Time RT-PCR was conducted to assess the expression of KLFs, cardiac commitment genes, inflammatory markers, and certain conduction-related genes. We devel-oped a computational approach to construct a proteomic network centered on KLFs. Initial results revealed early expression (2-3 days post-induction) of KLF3, KLF4 and KLF6, followed by the subsequent expression of KLF11 and KLF15 (5-8 days after induction). In the maturation stage, KLF12 and KLF13 regulators were found upregulated. IL-6 was gradually found to be upregulated through. Interaction analysis revealed KLF3, KLF8 and KLF12 interacted with cardiac electrical functions. RT-PCR confirmed up-regulation in cardiac genes linked to electrical function and scar maturation. Our findings underscore the central role of KLFs during the modulation of the cardiac hypertrophic response. Dysregulation of KLF expression resulted in damaged myocardium, participating in the progression of abnormal hypertrophy, highlighting their potential as therapeutic targets for heart diseases.

Cancer stem cells (CSCs) are a small subpopulation of cells within tumors with properties, such as self-renewal, differentiation, and tumorigenicity. CSCs have been proposed as a plausible therapeutic target as they are responsible for tumor recurrence, metastasis, and conventional therapy resistance. Selectively targeting CSCs is a promising strategy to eliminate the propagation of tumor cells and impair overall tumor development. Recent research shows that several immune cells play a crucial role in regulating tumor cell proliferation by regulating different CSC maintenance or proliferation pathways. There have been great advances in cellular immunotherapy using T cells, natural killer (NK) cells, macrophages, or stem cells for the selective targeting of tumor cells or CSCs in colorectal cancer (CRC). This review summarizes the CRC molecular profiles that may benefit from said therapy and the main vehicles used in cell therapy against CSCs. We also discuss the challenges, limitations, and advantages of combining conventional and/or current targeted treatments in the late stages of CRC.