细胞数量由细胞分裂和细胞死亡控制，其失调可能导致癌症等病理情况。为了维持细胞数量，称为凋亡的一种细胞淘汰过程也刺激了相邻细胞的增殖。这种凋亡诱导的代偿性增殖机制最初是在40年前描述的。虽然只有相邻的少数细胞需要分裂来补偿凋亡细胞的损失，但选择细胞分裂的机制一直未被揭示。在这里，我们发现相邻组织中是以Yes-associated protein (YAP)介导的机械转导的空间不均匀性决定了Madin-Darby犬肾细胞(MDCK)中代偿性增殖的不均匀性。这种不均匀性来自于核大小的不均匀分布和施加于相邻细胞的机械力的不均匀模式。我们从机械角度发现，这些结果为我们提供了关于组织如何精确维持稳态的更多见解。版权所有 ©2023 Elsevier Inc.。保留所有权利。

The number of cells in tissues is controlled by cell division and cell death, and its misregulation could lead to pathological conditions such as cancer. To maintain the cell numbers, a cell-elimination process called apoptosis also stimulates the proliferation of neighboring cells. This mechanism, apoptosis-induced compensatory proliferation, was originally described more than 40 years ago. Although only a limited number of the neighboring cells need to divide to compensate for the apoptotic cell loss, the mechanisms that select cells to divide have remained elusive. Here, we found that spatial inhomogeneity in Yes-associated protein (YAP)-mediated mechanotransduction in neighboring tissues determines the inhomogeneity of compensatory proliferation in Madin-Darby canine kidney (MDCK) cells. Such inhomogeneity arises from the non-uniform distribution of nuclear size and the non-uniform pattern of mechanical force applied to neighboring cells. Our findings from a mechanical perspective provide additional insight into how tissues precisely maintain homeostasis.Copyright © 2023 Elsevier Inc. All rights reserved.