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Understanding the role of PARP16 in the development of cardiac lipotoxicity

Implementing Organization

Indian Institute of Science
Principal Investigator
Dr. Ravi sundaresan Nagalingam
Indian Institute of Science
CO-Principal Investigator
Prof. sachin Kotak
Indian Institute of Science

About

Cardiovascular diseases (CVDs) are the leading cause of death worldwide, with a quarter of all deaths in India attributed to CVDs. Metabolic disorders like obesity, insulin resistance, and diabetes are characterized by dyslipidemia, which progresses to myocardial lipotoxicity and predisposes patients to heart failure. These syndromes have significant personal, social, and economic impacts, potentially affecting India's economic growth. Current therapeutic options treat symptoms, but insufficient understanding of the molecular players involved in heart failure's development and progression limits the development of novel therapeutics. Preliminary data shows a significant increase in PARP16 protein levels in the hearts of high fat diet-fed mice and db or db mice, which suffer from myocardial lipotoxicity. The proposed study aims to identify the role of PARP16 as a regulator of these pathways and investigate the molecular mechanisms by which it may be implicated in the development of cardiac lipotoxicity. The findings could provide novel insights into molecular players involved in cardiac lipotoxicity and identify key proteins that mediate cardiac metabolism, potentially serving as a potential therapeutic target for patients with metabolic comorbidities associated with heart failure.

Source

Source
science and Engineering Research Board (sERB), DsT
Funding Organization
Funding Organization
Anusandhan National Research Foundation (ANRF)
Quick Information
Area of Research
Life Sciences & Biotechnology
Focus Area
Cell Biology
Start Year
2024
End Year
2027
Sanction Amount
₹ 66.24 L
Status
Ongoing
Contact
rsundaresan@mcbl.iisc.ernet.in
Output
No. of Research Paper
00
Technologies (If Any)
00
No. of PhD Produced
00
No. of Patents
Filed : 00
Grant : 00
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