Cardiac fibroblasts play an important role in cardiac matrix turnover and are involved in cardiac fibrosis development. Ca²⁺ is a driving belt in this phenomenon. This study evaluates the functional expression and contribution of the Ca²⁺-activated channel TRPM4 in atrial fibroblast phenotype. Molecular and electrophysiological investigations were conducted in human atrial fibroblasts in primary culture and in atrial fibroblasts obtained from wild-type and transgenic mice with disrupted Trpm4 gene (Trpm4^−/−). A typical TRPM4 current was recorded on human cells (equal selectivity for Na⁺ and K⁺, activation by internal Ca²⁺, voltage sensitivity, conductance of 23.2 pS, inhibition by 9-phenanthrol (IC₅₀ = 6.1 × 10⁻⁶ mol L⁻¹)). Its detection rate was 13% on patches at days 2–4 in culture but raised to 100% on patches at day 28. By the same time, a cell growth was observed. This growth was smaller when cells were maintained in the presence of 9-phenanthrol. Similar cell growth was measured on wild-type mice atrial fibroblasts during culture. However, this growth was minimized on Trpm4^−/− mice fibroblasts compared to control animals. In addition, the expression of alpha smooth muscle actin increased during culture of atrial fibroblasts from wild-type mice. This was not observed in Trpm4^−/− mice fibroblasts. It is concluded that TRPM4 participates in fibroblast growth and could thus be involved in cardiac fibrosis.

心脏成纤维细胞在心脏基质转换中起重要作用，并参与心脏纤维化的发展。Ca ²⁺在这种现象中是驱动带。本研究评估了 Ca ²⁺激活的通道 TRPM4 在心房成纤维细胞表型中的功能表达和贡献。在原代培养的人心房成纤维细胞和从具有破坏的Trpm4基因 ( Trpm4 ^-/- ) 的野生型和转基因小鼠获得的心房成纤维细胞中进行了分子和电生理学研究。在人类细胞上记录了典型的 TRPM4 电流（对 Na ⁺和 K ^{+ 的}选择性相等，由内部 Ca ²⁺激活，电压敏感性，23.2 pS 的电导，9-菲酚的抑制作用（IC ₅₀  = 6.1 × 10 ^-6  mol L ^-1））。在培养的第 2-4 天，它在贴片上的检测率为 13%，但在第 28 天在贴片上的检测率提高到 100%。同时，观察到细胞生长。当细胞在 9-菲酚存在下维持时，这种生长较小。在培养期间在野生型小鼠心房成纤维细胞上测量了类似的细胞生长。然而，与对照动物相比，这种生长在Trpm4 ^-/-小鼠成纤维细胞上被最小化。此外，在培养来自野生型小鼠的心房成纤维细胞期间，α 平滑肌肌动蛋白的表达增加。这在Trpm4中没有观察到^-/-小鼠成纤维细胞。得出的结论是，TRPM4 参与成纤维细胞的生长，因此可能参与心脏纤维化。