Exploring TRPM7 Channel-Kinase for Disease Modulation: A Translational Approach.

INTRODUCTION This review examines the multifaceted involvement of the transient receptor potential melastatin-7 (TRPM7) channel-kinase in human disease and evaluates its suitability as a selective therapeutic target. Particular emphasis is placed on the integrated ion channel and serine/threonine kinase functions of TRPM7 and their contribution to pathogenic mechanisms across oncological, neurological, cardiovascular, and immunological disorders.

METHODS A structured survey of the literature published between 2010 and 2025 was undertaken using major biomedical databases. Evidence from molecular, cellular, experimental, and clinical investigations was synthesized, with specific attention to TRPM7-dependent regulation of cell proliferation, migration, apoptosis, and immune signaling.

RESULTS Collective findings identify TRPM7 as a key regulator of intracellular Mg2+ and Ca2+ homeostasis, thereby influencing multiple signaling pathways. Aberrant TRPM7 expression or activity is consistently associated with the onset and progression of diverse pathological conditions, including malignancy, neurodegeneration, cardiovascular dysfunction, and autoimmune disease. Pharmacological modulation of TRPM7 has demonstrated beneficial effects in preclinical models, supporting its therapeutic relevance.

DISCUSSION The distinctive channel-kinase architecture of TRPM7 enables coordinated control of ionic flux and phosphorylation-dependent signaling, positioning it at central nodes of inflammation, oxidative stress, and pathological cellular remodeling. Its context-dependent roles across tissues highlight opportunities for selective intervention.

CONCLUSION TRPM7 emerges as a pivotal mediator of disease-related signaling and a promising molecular target. Continued development of selective TRPM7 modulators may facilitate translation of mechanistic insights into clinically effective therapies.