Role of Semaphorin 3A in Kidney Development and Diseases.

acute kidney injury apoptosis chronic kidney injury diabetic nephropathy fibrosis inflammation lupus nephritis neuropilin-1 podocyte semaphorin 3A

Journal

Diagnostics (Basel, Switzerland)
ISSN: 2075-4418
Titre abrégé: Diagnostics (Basel)
Pays: Switzerland
ID NLM: 101658402

Informations de publication

Date de publication:
25 Sep 2023
Historique:
received: 23 08 2023
revised: 19 09 2023
accepted: 21 09 2023
medline: 14 10 2023
pubmed: 14 10 2023
entrez: 14 10 2023
Statut: epublish

Résumé

Kidney diseases are worldwide public health problems affecting millions of people. However, there are still limited therapeutic options against kidney diseases. Semaphorin 3A (SEMA3A) is a secreted and membrane-associated protein, which regulates diverse functions, including immune regulation, cell survival, migration and angiogenesis, thus involving in the several pathogeneses of diseases, including eyes and neurons, as well as kidneys. SEMA3A is expressed in podocytes and tubular cells in the normal adult kidney, and recent evidence has revealed that excess SEMA3A expression and the subsequent signaling pathway aggravate kidney injury in a variety of kidney diseases, including nephrotic syndrome, diabetic nephropathy, acute kidney injury, and chronic kidney disease. In addition, several reports have demonstrated that the inhibition of SEMA3A ameliorated kidney injury via a reduction in cell apoptosis, fibrosis and inflammation; thus, SEMA3A may be a potential therapeutic target for kidney diseases. In this review article, we summarized the current knowledge regarding the role of SEMA3A in kidney pathophysiology and their potential use in kidney diseases.

Identifiants

pubmed: 37835781
pii: diagnostics13193038
doi: 10.3390/diagnostics13193038
pmc: PMC10572269
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Subventions

Organisme : the Promotion of Science (JSPS)/Grants-in-Aid for Young Scientists
ID : 18K15978
Organisme : the Promotion of Science (JSPS)/Grants-in-Aid for Young Scientists
ID : 20K17283
Organisme : Shanghai Pujiang Young Rheumatologists Training Program
ID : SPROG2201

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Auteurs

Yizhen Sang (Y)

Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.
Department of Rheumatology and Immunology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.

Kenji Tsuji (K)

Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.

Hiroyuki Nakanoh (H)

Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.

Kazuhiko Fukushima (K)

Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.
Center for Systems Biology, Program in Membrane Biology, Division of Nephrology, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.

Shinji Kitamura (S)

Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.
Department of Nursing Science, Faculty of Health and Welfare Science, Okayama Prefectural University, Okayama 719-1197, Japan.

Jun Wada (J)

Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.

Classifications MeSH