2026-06-28T20:29:25Zhttps://docta.ucm.es/rest/oai/request
oai:docta.ucm.es:20.500.14352/1128692025-09-08T15:18:51Zcom_20.500.14352_14col_20.500.14352_15
Docta Complutense author Delgado Valero, Beatriz author De la Fuente Chávez, Lucia author Romero Miranda, Ana author Bartolomé Pascual, María Visitación author Ramchandani, Bunty author Islas, Fabian author Luaces Méndez, María author Cachofeiro Ramos, María Victoria author Martínez Martínez, Ernesto 2024-12-18T09:25:56Z 2024-12-18T09:25:56Z 2021 Delgado-Valero B, de la Fuente-Chávez L, Romero-Miranda A, Visitación Bartolomé M, Ramchandani B, Islas F, Luaces M, Cachofeiro V, Martínez-Martínez E. Role of endoplasmic reticulum stress in renal damage after myocardial infarction. Clin Sci (Lond). 2021 Jan 15;135(1):143-159. doi: 10.1042/CS20201137. PMID: 33355632. 10.1042/CS20201137 https://hdl.handle.net/20.500.14352/112869 https://doi.org/10.1042/CS20201137 https://pubmed.ncbi.nlm.nih.gov/33355632/ Myocardial infarction (MI) is associated with renal alterations resulting in poor outcomes in patients with MI. Renal fibrosis is a potent predictor of progression in patients and is often accompanied by inflammation and oxidative stress; however, the mechanisms involved in these alterations are not well established. Endoplasmic reticulum (ER) plays a central role in protein processing and folding. An accumulation of unfolded proteins leads to ER dysfunction, termed ER stress. Since the kidney is the organ with highest protein synthesis fractional rate, we herein investigated the effects of MI on ER stress at renal level, as well as the possible role of ER stress on renal alterations after MI. Patients and MI male Wistar rats showed an increase in the kidney injury marker neutrophil gelatinase-associated lipocalin (NGAL) at circulating level or renal level respectively. Four weeks post-MI rats presented renal fibrosis, oxidative stress and inflammation accompanied by ER stress activation characterized by enhanced immunoglobin binding protein (BiP), protein disulfide-isomerase A6 (PDIA6) and activating transcription factor 6-alpha (ATF6α) protein levels. In renal fibroblasts, palmitic acid (PA; 50-200 µM) and angiotensin II (Ang II; 10−8 to 10−6M) promoted extracellular matrix, superoxide anion production and inflammatory markers up-regulation. The presence of the ER stress inhibitor, 4-phenylbutyric acid (4-PBA; 4 µM), was able to prevent all of these modifications in renal cells. Therefore, the data show that ER stress mediates the deleterious effects of PA and Ang II in renal cells and support the potential role of ER stress on renal alterations associated with MI. eng Role of endoplasmic reticulum stress in renal damage after myocardial infarction journal article 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URL https://docta.ucm.es/bitstreams/53c6a784-1d41-46ac-a1b2-4ff241b2b87f/download File MD5 9063d42f2ea4a28a84cd49af6870236f 1689287 application/pdf Delgado-Valero B, et al. (2020). ER Stress in Renal Damage after MI. Clin Sci (Lond).pdf URL https://docta.ucm.es/bitstreams/ef642206-2f88-464b-85a0-2854aec6eff5/download File MD5 ebf20eb778f4719d3166b456d9f9fd59 67098 text/plain Delgado-Valero B, et al. (2020). ER Stress in Renal Damage after MI. Clin Sci (Lond).pdf.txt