Makoto Nakanishi

The paper identifies a treatment-resistant fibroblast state in RA synovitis that drives chronic inflammation through senescence-associated mechanisms and highlights therapeutic targets beyond cytokine inhibition.

This study uses a microfluidic model to show that senescent fibroblasts cause ECM softening through collagen network reorganization without changing permeability.

This study uses multi-omic profiling to show that senescent cells, particularly late myofibroblasts, transiently contribute to cardiac remodeling after myocardial infarction.

This study uses single-cell RNA sequencing to show that the GLS1 inhibitor BPTES eliminates inflammatory senescent cells in aged mice and reduces chronic inflammation.

This study identifies FBXO22 deficiency as a cause of a pleiotropic syndrome with growth restriction and neurodevelopmental delay, linked to an epigenetic signature involving histone demethylase KDM4B.

This study identifies CDCA7 as a hemimethylated DNA sensor that interacts with HELLS to facilitate nucleosome remodeling and DNA methylation maintenance.

This study compares the structural and functional differences between human and mouse DPPA3 in binding to UHRF1 PHD finger, showing weaker human DPPA3 binding and reduced inhibition of UHRF1 chromatin binding.

This study identifies USP7 and ATAD5 as key factors in terminating UHRF1-dependent PAF15 ubiquitin signaling, linking this process to the completion of maintenance DNA methylation.

The paper shows that PARP1-HPF1-dependent ADP-ribosylation recruits LIG3-XRCC1 to chromatin to mediate Okazaki fragment joining when LIG1 is absent.