The structure and composition of plant cell walls are modified to accommodate the needs of the cell and in response to environmental stimuli. Growth, development, and defense may demand potentially conflicting functional cell wall requirements, and thus modifications of the cell wall are tightly controlled in an adaptive manner. These modifications are mediated by a dedicated cell wall integrity (CWI) maintenance mechanism. We investigated the responses to cell wall damage (CWD) that compromise CWI and the underlying mechanisms in Arabidopsis thaliana. Inhibitor- and enzyme-triggered CWD induced similar, turgor-sensitive stress responses. Genetic analysis showed that the receptor-like kinase (RLK) FEI2 and the plasma membrane-localized mechano-sensitive Ca2+- channel MCA1 function downstream of the RLK THE1 in CWD perception. Phenotypic clustering with 27 genotypes identified a core group of RLKs and ion channels required for activation of CWD responses. In contrast, the responses were repressed by pattern-triggered immunity (PTI) signaling components including the receptors for plant elicitor peptides (AtPeps) PEPR1 and PEPR2 (PEPR1/2). Application of AtPep1 and AtPep3 repressed CWD-induced phytohormone accumulation in a concentration dependent manner. CWD induced the expression of both PROPEP1 and PROPEP3 as well as the release of a PROPEP3 fusion protein into the growth medium. These results suggest that AtPep-mediated signaling suppresses CWD-induced defense responses. If key PTI signaling elements acting downstream of PEPR1/2 are dysfunctional, suppression of CWD-induced responses is alleviated, thus compensating for the impairment.