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Decoding the enigma of cardiac arrhythmia and mechanosensitivity

Award Number: R35HL184262
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 08/01/2026
PERIOD OF PERFORMANCE END DATE: 07/31/2033

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Decoding the enigma of cardiac arrhythmia and mechanosensitivity - ABSTRACT Our laboratory was the first to demonstrate unequivocally that several isoforms of small conductance Ca2+- activated K+ channels (SK or KCa2 channels) underlie Ca2+-activated K+ current (IK,Ca) in cardiomyocytes. Since our original reports, knowledge of cardiac SK channels in the field has been greatly expanded. Studies by our group and more recently by others, have provided evidence to substantiate the important roles of SK channels in the heart. Interests in cardiac SK channels are further fueled by recent studies suggesting the possible roles of SK channels in human arrhythmias and atrial fibrillation (AF). Therefore, SK channel may represent a novel therapeutic target for atrial arrhythmias. Moreover, SK channels are the only known K+ channels upregulated in heart failure (HF), underpinning their importance in normal and diseased hearts. Significant gaps in our knowledge and seemingly contradictory findings on SK channel function in cardiac disease mechanisms are our motivations for the proposal. These challenges are: 1) Blockade of SK channels has been shown to be both anti-arrhythmic and proarrhythmic in various models; and 2) SK channels are upregulated in HF. However, the mechanisms for the observed upregulation remain incompletely understood. Thus, this multidisciplinary proposal will combine experimental and computational studies, taking advantage of complementary expertise from four different laboratories in structural, functional studies, optogenetic tools, and computational modeling to successively address the multifaceted SK channel remodeling in diseased hearts. The proposed study represents the necessary and critical steps to disentangle the highly complex SK channel remodeling in HF, the unique K+ channel that helps to compensate for the much-needed “repolarization reserve” in HF. Indeed, these knowledge gaps are extremely critical since SK channel inhibitors are currently under development for the treatment of AF. Our proposed studies are robust, leaving little doubt that the outcome would be rich in leaping the field forward.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $558,127 )
2026	2026	UNIVERSITY OF ARIZONA	845 N PARK AVE RM 538	TUCSON	AZ	85721	PIMA	USA	Cardiovascular Diseases Research	000	1	7/3/2026	NEW	$558,127
														Subtotal = $558,127

Grand Total All Awards = $558,127

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Decoding the enigma of cardiac arrhythmia and mechanosensitivity

Award Number: R35HL184262

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 08/01/2026

PERIOD OF PERFORMANCE END DATE: 07/31/2033

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