Publications

Nicotinamide adenine dinucleotide metabolism in the immuneresponse, autoimmunity and inflammageing

Navarro MN, Gómez de Las Heras MM, Mittelbrunn M.

Br J Pharmacol. 2022 May;

179(9):1839-1856.
doi: 10.1111/bph.15477.
PMID: 33817782 .

Metabolism is dynamically regulated to accompany immune cell function, and altered immunometabolism can result in impaired immune responses. Concomitantly, the pharmacological manipulation of metabolic processes offers an opportunity for therapeutic intervention in inflammatory disorders. The nicotinamide adenine dinucleotide (NAD+ ) is a critical metabolic intermediate that serves as enzyme cofactor in redox reactions, and is

Sexual dimorphism in the antitumor immune responses elicited by the combination of fasting and chemotherapy

Andrés Pastor-Fernández , Manuel Montero Gómez de Las Heras , Jose Ignacio Escrig-Larena , Marta Barradas , Cristina Pantoja, Adrian Plaza , Jose Luis Lopez-Aceituno , Esther Durán , Alejo Efeyan , Maria Mittelbrunn , Lola Martinez , Pablo Jose Fernandez-Marcos

DOI:10.1002/cac2.12535
PMID:38512765

 

 

Fasting reduces chemotherapy toxicity, enhances immunogenic tumor cell death and increases CD8+ T cell infiltration in tumors, particularly when combined with chemotherapy or immunotherapy. Moreover, fasting exhibits a sexual dimorphism in the immune system . The aim of our study was to elucidate the role of sex in the beneficial anti‐tumoral effects of combining fasting and

Galectin-1 prevents pathological vascular remodelingin atherosclerosis and abdominal aortic aneurysm

Roldán-Montero R, Pérez-Sáez JM, Cerro-Pardo I, Oller J, Martinez-Lopez D, Nuñez E, Maller SM, Gutierrez-Muñoz C, Mendez-Barbero N, Escola-Gil JC, Michel JB, Mittelbrunn M, Vázquez J, Blanco-Colio LM, Rabinovich GA, Martin-Ventura JL.

Sci Adv. 2022 Mar;

8(11):eabm7322.
doi: 10.1126/sciadv.abm7322.
PMID: 35294231

Pathological vascular remodeling is the underlying cause of atherosclerosis and abdominal aortic aneurysm (AAA). Here, we analyzed the role of galectin-1 (Gal-1), a 􀀀-galactoside–binding protein, as a therapeutic target for atherosclerosis and AAA. Mice lacking Gal-1 (Lgals1−/−) developed severe atherosclerosis induced by pAAV/D377Y-mPCSK9 adenovirus and displayed higher lipid levels and lower expression of contractile markers