Florence Malisan

Rome, 00133, Italy

Last Updated: 09/26/2026

Save publications for later

Sign Up

Not sure about your diagnosis?

Check Your Symptoms

Found 17 publications

Electromagnetic Transduction Therapy (EMTT) Enhances Tenocyte Regenerative Potential: Evidence for Senolytic-like Effects and Matrix Remodeling.

Electromagnetic Transduction Therapy (EMTT) Enhances Tenocyte Regenerative Potential: Evidence for Senolytic-like Effects and Matrix Remodeling.

Journal: International journal of molecular sciences

Published: May 15, 2025

An RNA-seq study in Friedreich ataxia patients identified hsa-miR-148a-3p as a putative prognostic biomarker of the disease.

An RNA-seq study in Friedreich ataxia patients identified hsa-miR-148a-3p as a putative prognostic biomarker of the disease.

Journal: Human genomics

Published: October 11, 2023

Interferon Gamma Enhances Cytoprotective Pathways via Nrf2 and MnSOD Induction in Friedreich's Ataxia Cells.

Interferon Gamma Enhances Cytoprotective Pathways via Nrf2 and MnSOD Induction in Friedreich's Ataxia Cells.

Journal: International journal of molecular sciences

Published: June 08, 2023

Drug Repositioning in Friedreich Ataxia.

Drug Repositioning in Friedreich Ataxia.

Journal: Frontiers in neuroscience

Published: November 13, 2021

Hsa-miR223-3p circulating level is upregulated in Friedreich's ataxia and inversely associated with HCLS1 associated protein X-1, HAX-1.

Hsa-miR223-3p circulating level is upregulated in Friedreich's ataxia and inversely associated with HCLS1 associated protein X-1, HAX-1.

Journal: Human molecular genetics

Published: July 30, 2021

Frataxin deficiency in Friedreich's ataxia is associated with reduced levels of HAX-1, a regulator of cardiomyocyte death and survival.

Frataxin deficiency in Friedreich's ataxia is associated with reduced levels of HAX-1, a regulator of cardiomyocyte death and survival.

Journal: Human molecular genetics

Published: August 05, 2019

Hyaluronic Acid (HA), Platelet-Rich Plasm and Extracorporeal Shock Wave Therapy (ESWT) promote human chondrocyte regeneration in vitro and ESWT-mediated increase of CD44 expression enhances their susceptibility to HA treatment.

Hyaluronic Acid (HA), Platelet-Rich Plasm and Extracorporeal Shock Wave Therapy (ESWT) promote human chondrocyte regeneration in vitro and ESWT-mediated increase of CD44 expression enhances their susceptibility to HA treatment.

Journal: PloS one

Published: January 21, 2019

Drug repositioning screening identifies etravirine as a potential therapeutic for friedreich's ataxia.

Drug repositioning screening identifies etravirine as a potential therapeutic for friedreich's ataxia.

Journal: Movement disorders : official journal of the Movement Disorder Society

Published: July 10, 2018

E3 Ligase RNF126 Directly Ubiquitinates Frataxin, Promoting Its Degradation: Identification of a Potential Therapeutic Target for Friedreich Ataxia.

E3 Ligase RNF126 Directly Ubiquitinates Frataxin, Promoting Its Degradation: Identification of a Potential Therapeutic Target for Friedreich Ataxia.

Journal: Cell reports

Published: August 10, 2016

Extracorporeal Shock Wave Treatment (ESWT) enhances the in vitro-induced differentiation of human tendon-derived stem/progenitor cells (hTSPCs).

Extracorporeal Shock Wave Treatment (ESWT) enhances the in vitro-induced differentiation of human tendon-derived stem/progenitor cells (hTSPCs).

Journal: Oncotarget

Published: August 03, 2015

Src inhibitors modulate frataxin protein levels.

Src inhibitors modulate frataxin protein levels.

Journal: Human molecular genetics

Published: December 30, 2014

Highly specific ubiquitin-competing molecules effectively promote frataxin accumulation and partially rescue the aconitase defect in Friedreich ataxia cells.

Highly specific ubiquitin-competing molecules effectively promote frataxin accumulation and partially rescue the aconitase defect in Friedreich ataxia cells.

Journal: Neurobiology of disease

Published: October 02, 2014

Showing 1-12 of 17

Last Updated: 09/26/2026